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The same combo i take.
Yes the CEO was sarcastic and was implying JT is clueless. Generics were mot surprised and thus never wanted to settle.
No but good confirmation
The virus has genome of HIV, ebola mixed in. Made made 100 percent.
Read carefully
2015 paper in Nature
Acknowledgements
Research in this manuscript was supported by grants from the National Institute of Allergy & Infectious Disease and the National Institute of Aging of the US National Institutes of Health (NIH) under awards U19AI109761 (R.S.B.), U19AI107810 (R.S.B.), AI085524 (W.A.M.), F32AI102561 (V.D.M.) and K99AG049092 (V.D.M.), and by the National Natural Science Foundation of China awards 81290341 (Z.-L.S.) and 31470260 (X.-Y.G.), and by USAID-EPT-PREDICT funding from EcoHealth Alliance (Z.-L.S.). Human airway epithelial cultures were supported by the National Institute of Diabetes and Digestive and Kidney Disease of the NIH under award NIH DK065988 (S.H.R.). We also thank M.T. Ferris (Dept. of Genetics, University of North Carolina) for the reviewing of statistical approaches and C.T. Tseng (Dept. of Microbiology and Immunology, University of Texas Medical Branch) for providing Calu-3 cells. Experiments with the full-length and chimeric SHC014 recombinant viruses were initiated and performed before the GOF research funding pause and have since been reviewed and approved for continued study by the NIH. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Author information
Affiliations
Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Vineet D Menachery, Boyd L Yount Jr, Kari Debbink, Lisa E Gralinski, Jessica A Plante, Rachel L Graham, Trevor Scobey, Eric F Donaldson & Ralph S Baric
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Kari Debbink & Ralph S Baric
National Center for Toxicological Research, Food and Drug Administration, Jefferson, Arkansas, USA
Sudhakar Agnihothram
Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China
Xing-Yi Ge & Zhengli-Li Shi
Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Scott H Randell
Cystic Fibrosis Center, Marsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Scott H Randell
Institute for Research in Biomedicine, Bellinzona Institute of Microbiology, Zurich, Switzerland
Antonio Lanzavecchia
Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA
Wayne A Marasco
Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
Wayne A Marasco
Contributions
V.D.M. designed, coordinated and performed experiments, completed analysis and wrote the manuscript. B.L.Y. designed the infectious clone and recovered chimeric viruses; S.A. completed neutralization assays; L.E.G. helped perform mouse experiments; T.S. and J.A.P. completed mouse experiments and plaque assays; X.-Y.G. performed pseudotyping experiments; K.D. generated structural figures and predictions; E.F.D. generated phylogenetic analysis; R.L.G. completed RNA analysis; S.H.R. provided primary HAE cultures; A.L. and W.A.M. provided critical monoclonal antibody reagents; and Z.-L.S. provided SHC014 spike sequences and plasmids. R.S.B. designed experiments and wrote manuscript.
Corresponding authors
Correspondence to Vineet D Menachery or Ralph S Baric.
Ethics declarations
Competing interests
The authors declare no competing financial interests.
From Nature paper
30 March 2020Editors’ note, March 2020: We are aware that this article is being used as the basis for unverified theories that the novel coronavirus causing COVID-19 was engineered. There is no evidence that this is true; scientists believe that an animal is the most likely source of the coronavirus.
Nothing to see here. Just look over-there. It is the wet market
Is that theory verified? How stupid is this statement.
All you need to do is to subpoena Dr Ralph Baric. The guy knows the real truth. Faucci knows the truth as well.
These crazy scientists published their corona virus “gain of function “ experiment in Nature in 2015.
Look at the authors, then scroll on the bottom and look at institutions that participated in this dumb research.
These people deserve to go to prison.
Yeah it emerged form the wet market. Lol. Sure it did.
Nature publication is here
https://www.nature.com/articles/nm.3985
I believe it can
My family eats only organic food. No pesticides. No junk food.
My wife had only mild covid infection. Few days of fever. No hypoxia.
I still feel genetics is the main factor. Even blood type plays a role
Type A bad
Type O better
We are still learning every day.
The sad thing is that this is created at University of North Carolina then transitioned to Wuhan lab, all paid by taxpayer money (NIH)
NIH gave 3.75 million dollars to Wuhan lab to continue the project.
https://www.thegatewaypundit.com/2020/04/huge-exclusive-chinese-doctor-shi-zhengli-ran-coronavirus-research-wuhan-us-project-shut-dhs-2014-risky-prior-leak-killed-researcher/
Thanks
Sorry for typo: meant to say “myself and my family get no influenza infection”.
Here is some material on flu vaccine efficacy
Efficacy — The efficacy of IIV in older adult patients has been evaluated in a few randomized trials [66-68] and multiple observational studies, both in the community and in long-term care facilities [69-79] as well as in sicker patients such as those with chronic lung disease [80-82], with conflicting results.
In a 2018 meta-analysis of randomized trials, IIV of older individuals resulted in less influenza over a single season than placebo (2.4 versus 6 percent; risk ratio [RR] 0.42, 95% CI 0.27-0.66) [83]. The authors rated the evidence as low certainty due to uncertainty about how influenza was diagnosed. One multicenter study suggested that influenza vaccine effectiveness decreases in older adults as frailty increases [84].
A 2008 case-control study evaluated 1173 cases and 2346 controls among community-dwelling older individuals during three pre-influenza periods and influenza seasons, periods when there was good antigenic match between the influenza vaccine and circulating viruses [75]. This study found that influenza vaccination did not reduce the risk of pneumonia (including those who did not require hospitalization), after adjusting for the presence and severity of comorbidities. In contrast, in a 2012 cohort study of community-dwelling older individuals that evaluated 12.6 million person-influenza seasons, vaccination was associated with a reduction in the composite endpoint of hospitalization (for pneumonia and influenza) and death during influenza season (aOR 0.86, 95% CI 0.79-0.92) [85]. A case-control study also showed that influenza vaccination was associated with a significant reduction in the risk of hospitalization due to laboratory-confirmed influenza among adults aged ≥50 years of age regardless of age group (50 to <65 years; 65 to <75 years; ≥75 years) [86]. In another study of older individuals, vaccination was 58 percent effective at preventing medically attending laboratory-confirmed influenza illness in adults ≥50 years of age as well as in adults ≥65 years of age [87]. Influenza vaccination has also been associated with reduced risk of postoperative pneumonia among patients >66 years of age who underwent major surgery [88].
Even when vaccine efficacy is low, vaccination is likely to prevent hospitalizations in the older adult population. In a modeling study, during the 2012 to 2013 influenza season (a moderate to severe season), among individuals ≥65 years of age in the United States, a vaccine with 10 percent effectiveness and 66 percent coverage would have averted approximately 13,000 hospitalizations and a vaccine with 40 percent effectiveness would have averted approximately 60,000 hospitalizations [89]. In a population-based study in the United States that assessed the effect of influenza vaccination on disease severity among hospitalized patients ≥65 years of age during the 2013 to 2014 influenza season, a season in which vaccine viruses were antigenically similar to circulating viruses, influenza vaccination was associated with reduced risk of ICU admission and in-hospital mortality as well as reduced ICU and hospital length of stay [46].
Since protection against influenza is suboptimal in older adults, it is not surprising that the outbreaks of influenza have occurred in nursing homes where 80 to 98 percent of residents were vaccinated [74].
Vaccinating younger adults appears to provide benefit for older adults in the same community. In a large nationwide sample of Medicare beneficiaries in the United States, vaccination of adults aged 18 to 64 years was inversely associated with influenza-related illness in individuals ≥65 years of age [90].
Effect of statins — Statins are used commonly in older adults with hyperlipidemia and are known to have immunomodulatory effects, which could affect vaccine responses. In an observational study conducted in the context of a randomized trial that evaluated influenza vaccines in individuals >65 years of age, hemagglutination inhibition (HAI) geometric mean titers to various influenza strains were 38 to 67 percent lower in those receiving chronic statin therapy than in those not receiving it [91]. In addition, in a large retrospective cohort study conducted over nine influenza seasons in the United States, statin use was associated with reduced influenza vaccine effectiveness against medically attended acute respiratory illness [92]. In an adjusted analysis, influenza vaccine effectiveness against medically attended acute respiratory illness was lower among statin users than statin nonusers during periods of local (14.1 versus 22.9 percent; mean difference 11.4 percent, 95% CI -1.7 to 26.1 percent) and widespread (12.6 versus 26.2 percent; mean difference 18.4 percent, 95% CI 2.9 to 36.2 percent) influenza virus circulation. In a prospective study, statin use reduced the effectiveness of influenza vaccination against laboratory-confirmed H3N2 influenza A but not against H1N1 influenza A or influenza B [93]. In contrast, in a retrospective cohort study of 2.8 million Medicare beneficiaries in the United States, statin use around the time of high-dose or standard-dose vaccination did not substantially affect the risk of influenza-related visits or influenza-related hospitalizations [94]. In a large observational study over six influenza seasons, influenza vaccine effectiveness was not affected by statin use [95].
The observed associations between statin use and reduced vaccine effectiveness in some studies could be due to confounding, as patients who are being treated with statins are likely to be at differing baseline risk of influenza from those not treated with statins. Although these studies raise the possibility that older patients receiving statins are less likely to be protected by the influenza vaccine than those not receiving statins, such individuals should still receive statins, when indicated, as well as an influenza vaccine (preferably the high-dose vaccine) annually. (See 'Choice of vaccine formulation' above.)
Effect on mortality — It has been difficult to demonstrate an improvement in survival after influenza vaccination in older adult patients in randomized trials because mortality is a rare endpoint. Some studies have observed a significant reduction in death from influenza or pneumonia [96], but some experts have suggested that frailty selection bias in cohort studies has led to an overestimation of any mortality benefit of influenza vaccination in older adults [97]. The following studies illustrate the range of findings and some of the limitations in study design:
?A pooled cohort study demonstrated a small but significant reduction in mortality in vaccinated older individuals (1.0 versus 1.6 percent in unvaccinated individuals) [70]. A sensitivity analysis was performed to detect unmeasured confounders. Even when a higher rate of confounders was assumed, there was still a significant reduction in mortality. Other studies have supported this finding [98].
?The difficulty of using observational data to evaluate the effect of influenza vaccine on mortality is illustrated by a prospective case-control study of patients (mostly over the age of 65) with CAP. The study assessed the impact of influenza vaccination on in-hospital mortality in patients admitted during the off-season for influenza [99]. A significant mortality reduction was observed in vaccinated patients (odds ratio [OR] 0.49, 95% CI 0.30-0.79). However, when adjustments were made to address confounding factors (eg, functional and socioeconomic status), the mortality benefit became nonsignificant (aOR 0.81, 95% CI 0.35-1.85). This study shows that the presence of bias may overestimate the mortality benefit of influenza vaccination [100].
?A large cohort study of community-dwelling older individuals did not detect a mortality benefit from influenza vaccination [85]. An important limitation of this study was the likely underreporting of vaccination status, which could have contributed to the vaccine appearing ineffective [101].
?In a population-based study in the United States, influenza vaccination was associated with reduced risk of in-hospital death among individuals ≥65 years of age [46].
?In a matched cohort study of patients >66 years of age in Taiwan, those who received the influenza vaccine and later underwent major surgery had lower in-hospital mortality than unvaccinated patients (OR 0.46, 95% CI 0.39-0.56) [88].
?Annual revaccination has been associated with a reduction in mortality in older adults. A report from the Netherlands of over 26,000 community-dwelling older individuals evaluated the association between the number of consecutive annual influenza vaccinations and all-cause mortality [29]. After adjustment for age, sex, and comorbidities, the following findings were noted:
•A first vaccination was associated with a nonsignificant annual reduction in mortality risk of 10 percent, while revaccination was associated with a significant 24 percent reduction in mortality overall and a 28 percent reduction during epidemics. There was also a trend toward further benefit with each consecutive vaccination.
•Vaccination interruption was associated with a strong and significant increase in mortality risk (adjusted hazard ratio [HR] 1.25, 95% CI 1.10-1.42), an effect that was reversed with restarting annual vaccination.
The impact of the high-dose vaccine on mortality is discussed below. (See 'High-dose vaccine' below.)
High-dose vaccine — A high-dose trivalent inactivated influenza vaccine, Fluzone High-Dose, is approved for individuals ≥65 years of age [15]. The high-dose vaccine contains 60 mcg of hemagglutinin per strain, whereas the standard-dose vaccine contain 15 mcg per strain (see 'Choice of vaccine formulation' above). The high-dose trivalent inactivated vaccine is more immunogenic and effective than the standard-dose trivalent inactivated vaccine (including a mortality benefit) in older patients, but it has not been compared directly to the standard-dose quadrivalent inactivated vaccine.
In a multicenter trial that included 31,989 adults ≥65 years of age, Fluzone High-Dose was modestly more effective than standard-dose trivalent Fluzone [102]. In the intention-to-treat analysis, 228 individuals in the high-dose group (1.4 percent) and 301 in the standard-dose group (1.9 percent) had laboratory-confirmed influenza associated with an influenza-like illness (relative efficacy 24.2 percent, 95% CI 9.7 to 36.5 percent). After vaccination, HAI titers and seroprotection rates (the percentage of participants with HAI titers ≥1:40) were higher in the high-dose group. At least one serious adverse event was reported in 8.3 percent of individuals who received the high-dose vaccine compared with 9.0 percent of those who received the standard-dose vaccine. Three recipients of the high-dose vaccine had serious adverse events classified as related to vaccination (cranial nerve VI palsy starting one day after vaccination; hypovolemic shock associated with diarrhea starting one day after vaccination; acute disseminated encephalomyelitis starting 117 days after vaccination); all three events resolved before study completion. Continued postmarketing surveillance will be necessary to detect potential rare but serious adverse events. The incidence of mild to moderate local reactions was not reported.
A study of >6 million United States Medicare beneficiaries ≥65 years of age who received either the high-dose or the standard-dose trivalent influenza vaccine during the 2012 to 2013 or 2013 to 2014 influenza seasons evaluated the comparative effectiveness (CE) of the two vaccines; the vaccines were well-matched to the circulating strains during both seasons [103]. The primary outcome was death during the 30 days following an inpatient or emergency department encounter listing an influenza diagnostic code. The mortality rate was 0.028 per 10,000 person-weeks for the high-dose vaccine compared with 0.038 per 10,000 person-weeks for the standard-dose vaccine; overall CE was 24 percent (95% CI 0.6 to 42 percent). The high-dose vaccine was more effective than the standard-dose vaccine for preventing postinfluenza death during the 2012 to 2013 influenza season (36.4 percent CE, 95% CI 9 to 56 percent), a season when circulation of H3N2 influenza A (a strain associated with severe disease) was common. In contrast, it was not more effective for preventing postinfluenza death during the following season (2.5 percent CE, 95% CI -47 to 35 percent), when H1N1 influenza A (a strain associated with mild disease) predominated. It is likely that the difference between the results for the two seasons was due to the fact that it is difficult to demonstrate benefit during a mild influenza season, when death is a rare outcome. The high-dose vaccine was associated with a reduced risk of hospitalization during both seasons (2012 to 2013 CE 22.1 percent, 95% CI 16.6 to 27.3 percent; 2013 to 2014 CE 12.7 percent, 95% CI 4.9 to 19.9 percent).
In a cluster-randomized trial that compared the high-dose vaccine to a standard-dose trivalent vaccine in residents ≥65 years of age in 823 nursing homes in the United States, the incidence of respiratory-related hospital admissions was lower in facilities where residents received high-dose vaccine than in those where residents received standard-dose vaccine (adjusted relative risk 0.87, 95% CI 0.78-0.98) [104].
Further, in a retrospective cohort study that evaluated >19 million United States Medicare beneficiaries ≥65 years of age who received either the high-dose or the standard-dose influenza vaccine during six influenza seasons between 2012 and 2018, the high-dose vaccine was more effective than standard-dose vaccines in preventing influenza-related hospital encounters (influenza-related inpatient stays and emergency department visits) in four of the six influenza seasons evaluated and was at least as effective in the other two seasons [105]. The high-dose vaccine was consistently more effective than standard-dose vaccines across all seasons for individuals aged ≥85 years of age. Similarly, the high-dose vaccine was more effective than the standard-dose vaccine at protecting veterans ≥65 years of age in the United States against influenza- or pneumonia-associated hospitalization [106]. In contrast, in another large retrospective cohort study of veterans ≥65 years of age in the United States, the high-dose vaccine was not more effective than standard-dose vaccine in protecting against hospitalization for influenza or pneumonia except in those ≥85 years of age [107].
There is also evidence that the high-dose vaccine is more immunogenic than the standard-dose trivalent vaccine in older adults [108-110]. Mild to moderate local reactions are more common in those who receive the high-dose vaccine than the standard-dose vaccine [108].
The high-dose influenza vaccine is more expensive than the standard-dose trivalent vaccine. However, in a cost analysis of data from the trial in individuals ≥65 years of age that found that the high-dose vaccine was effective [102], the high-dose influenza vaccine appeared likely to result in cost savings compared with the standard-dose vaccine [111].
A high-dose quadrivalent vaccine was approved by the FDA in November 2019 for individuals ≥65 years of age and is expected to be available for the 2020 to 2021 influenza season in the United States [16]. In a randomized trial that compared the high-dose quadrivalent vaccine with the high-dose trivalent vaccine in individuals ≥65 years of age, the quadrivalent vaccine resulted in improved immunogenicity against the added strain without reducing the immunogenicity of the other strains [112]. The proportion of individuals who had injection site pain, myalgia, malaise, or headache was slightly higher in the quadrivalent vaccine group than in the trivalent vaccine group.
The immunogenicity of the high-dose vaccine in HIV-infected individuals is discussed separately. (See "Immunizations in patients with HIV", section on 'Efficacy, immunogenicity, and safety'.)
Recombinant hemagglutinin vaccine — As noted above, the FDA has approved a quadrivalent recombinant HA influenza vaccine (Flublok Quadrivalent) for individuals 18 years of age or older; the vaccine is produced using recombinant DNA technology and a baculovirus expression system that produces virus-like particles [54,55]. (See 'Vaccine formulations' above.)
In a randomized trial that included 9003 adults ≥50 years of age, Flublok Quadrivalent (45 mcg of recombinant HA per strain) was compared with a quadrivalent formulation of a standard-dose inactivated influenza vaccine (15 mcg of HA per strain) [113]. In the modified intention-to-treat population, the polymerase chain reaction (PCR)-confirmed influenza attack rate was 2.2 percent with Flublok Quadrivalent compared with 3.1 percent with the inactivated vaccine. The cumulative incidence of PCR-confirmed influenza-like illness was 30 percent lower with Flublok Quadrivalent than with the inactivated vaccine (hazard ratio [HR] 0.69, 95% CI 0.53-0.90). In a post-hoc analysis, Flublok Quadrivalent had a relative vaccine efficacy of 36 percent against influenza A compared with the inactivated vaccine (HR 0.64, 95% 0.48-0.86), but the two vaccines had similar efficacy against influenza B. Flublok Quadrivalent has not been compared directly with the high-dose inactivated vaccine, which has been found to be more effective than the standard dose inactivated vaccine in older adults. (See 'High-dose vaccine' above.)
I do because it is required to get a flu shot if you work at a hospital. The other option was to wear a mask for 6 months each year. My family doesn’t get a flu shot. Er get mo flu infections either.
As far as covid, i feel the individual immunity strength and weakness, all determined by genetics, play a huge role who gets mild symptoms and who gets really sick.
Well...
Many years of use with no significant side effects. Flu shot should be ok as it is proven to be safe.
My problem with flu shot: depending on a specific year, it may be 30 to 50 percent effective.
Covid 19 vaccine needs several years of use to determine real safety.
Merck says it is safe
I say bullshit
https://www.webmd.com/cancer/cervical-cancer/news/20090430/gardasil-linked-to-nerve-disorder
How about paralysis (GB syndrome)
You get it and you stay paralyzed
Multiple cases in South America
https://health.usnews.com/health-news/blogs/on-women/2009/03/20/cdc-takes-closer-look-at-gardasil-and-paralysis
Gardisil
Postmarketing:
Cardiovascular: Syncope
Dermatologic: Urticaria
Gastrointestinal: Vomiting
Contraindications
Hypersensitivity, including severe allergic reactions to yeast (a vaccine component), or after a previous dose of this vaccine or human papillomavirus (types 6, 11, 16, 18) vaccine (recombinant).
Warnings/Precautions
Concerns related to adverse effects:
• Anaphylactoid/hypersensitivity reactions: Immediate treatment (including epinephrine 1 mg/mL) for anaphylactoid and/or hypersensitivity reactions should be available during vaccine use (ACIP [Ezeanolue 2020]).
• Shoulder injury related to vaccine administration: Vaccine administration that is too high on the upper arm may cause shoulder injury (eg, shoulder bursitis or tendinitis) resulting in shoulder pain and reduced range of motion following injection. Use proper injection technique for vaccines administered in the deltoid muscle (eg, injecting in the central, thickest part of the muscle) to reduce the risk of shoulder injury related to vaccine administration (Cross 2016; Foster 2013).
• Syncope: Syncope has been reported with use of injectable vaccines and may result in serious secondary injury (eg, skull fracture, cerebral hemorrhage); typically reported in adolescents and young adults and within 15 minutes after vaccination. Procedures should be in place to avoid injuries from falling and to restore cerebral perfusion if syncope occurs (ACIP [Ezeanolue 2020]).
Many approved drugs, felt to be safe, exhibited new side effect after approval.
PSG has a very powerful team They have a chance. But remember what Gary Lineker said:
Football is a simple game. Twenty-two men chase a ball for 90 minutes and at the end, the Germans always win.
Please don’t say soccer when you know it is football.
My prediction: Bayern wins
If i am intubated...yes. Lol
They are rushing the vaccine. It may not be safe. I will wait for few years.
All i know is i am not putting that vaccine into my body at least for now. Will wait for 3 years to evaluate the safety. Don’t trust it. I would rather get Covid than vaccine.
Why waste time? Nobody knows anything. Just wait for the decision.
Ask him? How else would you know?you cannot expect us to know what Singers’ motivations are? You have to ask him. Or to listen to his conversations and deduct it that way.
My opinion: he wants to win and improve the score 10 to 8 or 80 percent case win.
Are we at $200 yet? :)
Myocarditis occurs in covid but respiratory failure/hypoxia/pneumonia is the most common.
I do. I have been uptodate subscriber for many years. It is on my phone.
But this is not research. This is literature and topic review.
So...based on the latest literature review:
Pneumonia appears to be the most frequent serious manifestation of infection, characterized primarily by fever, cough, dyspnea, and bilateral infiltrates on chest imaging [23-25,77]
That is based in current literature.
The heart is impacted but nowhere near the lungs.
References
Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020; 395:497.
Chen N, Zhou M, Dong X, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet 2020; 395:507.
Wang D, Hu B, Hu C, et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA 2020.
Guan WJ, Ni ZY, Hu Y, et al. Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med 2020; 382:1708.
I have resources you don’t.
What does it say here:
This topic last updated: Aug 14, 2020.
That means that all relevant medical literature has been reviewed and updated 2 days ago.
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2020. | This topic last updated: Aug 14, 2020.
Author:Kenneth McIntosh, MDSection Editor:Martin S Hirsch, MDDeputy Editor:Allyson Bloom, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2020. | This topic last updated: Aug 14, 2020.
INTRODUCTION
Coronaviruses are important human and animal pathogens. At the end of 2019, a novel coronavirus was identified as the cause of a cluster of pneumonia cases in Wuhan, a city in the Hubei Province of China. It rapidly spread, resulting in an epidemic throughout China, followed by an increasing number of cases in other countries throughout the world. In February 2020, the World Health Organization designated the disease COVID-19, which stands for coronavirus disease 2019 [1]. The virus that causes COVID-19 is designated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); previously, it was referred to as 2019-nCoV.
Understanding of COVID-19 is evolving. Interim guidance has been issued by the World Health Organization and by the United States Centers for Disease Control and Prevention [2,3]. Links to these and other related society guidelines are found elsewhere. (See "Coronavirus disease 2019 (COVID-19): Epidemiology, virology, and prevention", section on 'Society guideline links'.)
This topic will discuss the clinical features of COVID-19. The epidemiology, virology, prevention, and diagnosis of COVID-19 are discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Epidemiology, virology, and prevention" and "Coronavirus disease 2019 (COVID-19): Diagnosis".)
The management of COVID-19 is also discussed in detail elsewhere:
?(See "Coronavirus disease 2019 (COVID-19): Outpatient evaluation and management in adults".)
?(See "Coronavirus disease 2019 (COVID-19): Management in hospitalized adults".)
?(See "Coronavirus disease 2019 (COVID-19): Infection control in health care and home settings".)
Issues related to COVID-19 in pregnant women and children are discussed elsewhere:
?(See "Coronavirus disease 2019 (COVID-19): Pregnancy issues".)
?(See "Coronavirus disease 2019 (COVID-19): Clinical manifestations and diagnosis in children" and "Coronavirus disease 2019 (COVID-19): Multisystem inflammatory syndrome in children".)
See specific topic reviews for details on complications of COVID-19 and issues related to COVID-19 in other patient populations.
Common cold coronaviruses, severe acute respiratory syndrome (SARS) coronavirus, and Middle East respiratory syndrome (MERS) coronavirus are discussed separately. (See "Coronaviruses" and "Severe acute respiratory syndrome (SARS)" and "Middle East respiratory syndrome coronavirus: Virology, pathogenesis, and epidemiology".)
ASYMPTOMATIC INFECTIONS
Asymptomatic infections have been well documented [4-12]. The proportion of infections that are asymptomatic has not been systematically and prospectively studied. One literature review estimated that it is as high as 30 to 40 percent, based on data from three large cohorts that identified cases through population-based testing [12,13]. However, in most of these and other studies, longitudinal follow-up to assess for symptom development was not performed. Additionally, the definition of "asymptomatic" may vary across studies, depending on which specific symptoms were assessed. The range of findings in studies evaluating asymptomatic infections is reflected in the following examples:
?In a COVID-19 outbreak on a cruise ship where nearly all passengers and staff were screened for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), approximately 19 percent of the population on board tested positive ; 58 percent of the 712 confirmed COVID-19 cases were asymptomatic at the time of diagnosis [14,15]. In studies of subsets of those asymptomatic individuals, who were hospitalized and monitored, approximately 77 to 89 percent remained asymptomatic over time [15,16].
?In a smaller COVID-19 outbreak within a skilled nursing facility, 27 of the 48 residents (56 percent) who had a positive screening test were asymptomatic at the time of diagnosis, but 24 of them ultimately developed symptoms over the next seven days [17].
?Other studies have reported even higher proportions of asymptomatic cases [10,18-20]. As an example, in a report of a universal screening program of pregnant women presenting for delivery at two New York hospitals at the height of the pandemic there, 29 of 210 asymptomatic women without fever (14 percent) had a positive SARS-CoV-2 reverse-transcription polymerase chain reaction (RT-PCR) test on a nasopharyngeal specimen [10]. Four additional women had fever or symptoms and also tested positive. Thus, of 33 women with a positive SARS-CoV-2 test, 29 (88 percent) were asymptomatic on presentation.
Even patients with asymptomatic infection may have objective clinical abnormalities [9,21]. As an example, in a study of 24 patients with asymptomatic infection who all underwent chest computed tomography (CT), 50 percent had typical ground-glass opacities or patchy shadowing, and another 20 percent had atypical imaging abnormalities [21]. Five patients developed low-grade fever, with or without other typical symptoms, a few days after diagnosis. In another study of 55 patients with asymptomatic infection identified through contact tracing, 67 percent had CT evidence of pneumonia on admission; only two patients developed hypoxia, and all recovered [9].
As above, some individuals who are asymptomatic at the time of diagnosis go on to develop symptoms (ie, they were actually presymptomatic). In one study, symptom onset occurred a median of four days (range of three to seven) after the initial positive RT-PCR test [15].
The risk of transmission from patients with asymptomatic infection is discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Epidemiology, virology, and prevention", section on 'Viral shedding and period of infectiousness'.)
SEVERITY OF SYMPTOMATIC INFECTION
Spectrum of severity and case fatality rates — The spectrum of symptomatic infection ranges from mild to critical; most infections are not severe [4,22-27]. Specifically, in a report from the Chinese Center for Disease Control and Prevention that included approximately 44,500 confirmed infections with an estimation of disease severity [28]:
?Mild (no or mild pneumonia) was reported in 81 percent.
?Severe disease (eg, with dyspnea, hypoxia, or >50 percent lung involvement on imaging within 24 to 48 hours) was reported in 14 percent.
?Critical disease (eg, with respiratory failure, shock, or multiorgan dysfunction) was reported in 5 percent.
?The overall case fatality rate was 2.3 percent; no deaths were reported among noncritical cases.
Among hospitalized patients, the proportion of critical or fatal disease is higher [29-35]. In a study that included 2741 patients who were hospitalized for COVID-19 in a New York City health care system, 665 patients (24 percent) died or were discharged to hospice, including 241 who were not treated in an intensive care unit [32]. Of the 749 patients who received intensive care (27 percent of the total hospitalized cohort), 647 received invasive mechanical ventilation; of those patients, 60 percent died, 13 percent were still ventilated, and 16 percent were discharged.
The proportion of severe or fatal infections may also vary by location. According to a joint World Health Organization (WHO)-China fact-finding mission, the case fatality rate ranged from 5.8 percent in Wuhan to 0.7 percent in the rest of China [36]. A modeling study suggested that the adjusted case fatality rate in mainland China was 1.4 percent [37]. Most of the fatal cases occurred in patients with advanced age or underlying medical comorbidities [28,38]. In Italy, 12 percent of all detected COVID-19 cases and 16 percent of all hospitalized patients were admitted to the intensive care unit; the estimated case fatality rate was 7.2 percent in mid-March [39,40]. In contrast, the estimated case fatality rate in mid-March in South Korea was 0.9 percent [41]. This may be related to distinct demographics of infection; in Italy, the median age of patients with infection was 64 years, whereas in Korea, the median age was in the 40s. (See 'Impact of age' below.)
The case fatality rate only indicates the mortality rate among documented cases. Since many SARS-CoV-2 infections are asymptomatic, the infection fatality rate (ie, the estimated mortality rate among all individuals with infection) is considerably lower and has been estimated by some analyses to be between 0.5 and 1 percent [42,43]. Conversely, the reported case fatality rates are likely underestimates of the true case fatality rates, as many fatal infections are undiagnosed [44]. Neither the case fatality rate nor the infection fatality rate account for the full burden of the pandemic, which includes excess mortality from other conditions because of delayed care, overburdened health care systems, and social determinants of health [45].
Risk factors for severe illness — Severe illness can occur in otherwise healthy individuals of any age, but it predominantly occurs in adults with advanced age or underlying medical comorbidities. The impact of age is discussed elsewhere. (See 'Impact of age' below.)
Comorbidities and other conditions that have been associated with severe illness and mortality include [28,32,38,46-50]:
?Cardiovascular disease
?Diabetes mellitus
?Hypertension
?Chronic lung disease
?Cancer (in particular hematologic malignancies, lung cancer, and metastatic disease) [51]
?Chronic kidney disease
?Obesity
?Smoking
The United States Centers for Disease Control and Prevention (CDC) has created a list of certain comorbidities that have been associated with severe disease (defined as infection resulting in hospitalization, admission to the intensive care unit [ICU], intubation or mechanical ventilation, or death) and notes that the strength of evidence informing the associations varies [52]. These comorbidities are outlined in the table (table 1).
In a report of 355 patients who died with COVID-19 in Italy, the mean number of pre-existing comorbidities was 2.7, and only 3 patients had no underlying condition [40].
Among patients with advanced age and medical comorbidities, COVID-19 is frequently severe. For example, in a SARS-CoV-2 outbreak across several long-term care facilities in Washington State, the median age of the 101 facility residents affected was 83 years, and 94 percent had a chronic underlying condition; the hospitalization and preliminary case fatality rates were 55 and 34 percent, respectively [53]. In an analysis of nearly 300,000 confirmed COVID-19 cases reported in the United States, the mortality rate was 12 times as high among patients with reported co-morbidities compared with those with none [54].
Certain demographic features have also been associated with more severe illness. Males have comprised a disproportionately high number of deaths in cohorts from China, Italy, Denmark, and the United States [29,32,40,55,56]. Individuals of non-white race, specifically Black, Hispanic, and South Asian individuals, comprise a disproportionately high number of infections and deaths due to COVID-19 in the United States and United Kingdom, likely related to underlying disparities in the social determinants of health [49,57-60].
Particular laboratory features have also been associated with worse outcomes (table 2). These include [38,61-63]:
?Lymphopenia
?Thrombocytopenia
?Elevated liver enzymes
?Elevated lactate dehydrogenase (LDH)
?Elevated inflammatory markers (eg, C-reactive protein [CRP], ferritin)
?Elevated D-dimer (>1 mcg/mL)
?Elevated prothrombin time (PT)
?Elevated troponin
?Elevated creatine phosphokinase (CPK)
?Acute kidney injury
As an example, in one study, progressive decline in the lymphocyte count and rise in the D-dimer over time were observed in nonsurvivors compared with more stable levels in survivors [25].
Host genetic factors are also being evaluated for associations with severe disease [64,65]. As an example, one genome-wide association study identified a relationship between polymorphisms in the genes encoding the ABO blood group and respiratory failure from COVID-19 (type A associated with a higher risk) [64].
Patients with severe disease have also been reported to have higher viral RNA levels in respiratory specimens than those with milder disease [66,67], although this association was not observed in a different study that measured viral RNA in salivary specimens [68]. Detection of viral RNA in the blood has been associated with organ damage (eg, lung, heart, kidney), coagulopathy, and mortality [69].
Several prediction tools have been proposed to identify patients who are more likely to have severe illness based on epidemiologic, clinical, and laboratory features; however, most of the studies evaluating these tools are limited by risk of bias, and none has been prospectively evaluated or validated for clinical management [70].
Impact of age — Individuals of any age can acquire severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, although adults of middle age and older are most commonly affected, and older adults are more likely to have severe disease.
In several cohorts of hospitalized patients with confirmed COVID-19, the median age ranged from 49 to 56 years [23-25]. In a report from the Chinese Center for Disease Control and Prevention that included approximately 44,500 confirmed infections, 87 percent of patients were between 30 and 79 years old [28]. Similarly, in a modeling study based on data from mainland China, the hospitalization rate for COVID-19 increased with age, with a 1 percent rate for those 20 to 29 years old, 4 percent rate for those 50 to 59 years old, and 18 percent for those older than 80 years [37].
Older age is also associated with increased mortality [28,29,40,49]. In a report from the Chinese Center for Disease Control and Prevention, case fatality rates were 8 and 15 percent among those aged 70 to 79 years and 80 years or older, respectively, in contrast to the 2.3 percent case fatality rate among the entire cohort [28]. In an analysis from the United Kingdom, the risk of death among individuals 80 years and older was 20-fold that among individuals 50 to 59 years old [49].
In the United States, 2449 patients diagnosed with COVID-19 between February 12 and March 16, 2020 had age, hospitalization, and ICU information available [71]; 67 percent of cases were diagnosed in those aged ≥45 years, and, similar to findings from China, mortality was highest among older individuals, with 80 percent of deaths occurring in those aged ≥65 years.
Symptomatic infection in children and adolescents appears to be relatively uncommon; when it occurs, it is usually mild, although severe cases and complications have been reported [72-75]. Details of COVID-19 in children are discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Clinical manifestations and diagnosis in children".)
CLINICAL MANIFESTATIONS
Incubation period — The incubation period for COVID-19 is generally within 14 days following exposure, with most cases occurring approximately four to five days after exposure [4,76,77].
In a study of 1099 patients with confirmed symptomatic COVID-19, the median incubation period was four days (interquartile range two to seven days) [77]. Using data from 181 confirmed cases in China with identifiable exposure, one modeling study estimated that symptoms would develop in 2.5 percent of infected individuals within 2.2 days and in 97.5 percent of infected individuals within 11.5 days [78]. The median incubation period in this study was 5.1 days.
However, determinations of the incubation period can be imprecise and may differ by the method of assessing exposure and the specific calculations used for the estimate. Another study estimated incubation period using data from 1084 patients who had traveled or resided in Wuhan and were subsequently diagnosed with COVID-19 after leaving Wuhan [79]. This study suggested a longer median incubation period of 7.8 days, with 5 to 10 percent of individuals developing symptoms 14 days or more after exposure.
Initial presentation — Pneumonia appears to be the most frequent serious manifestation of infection, characterized primarily by fever, cough, dyspnea, and bilateral infiltrates on chest imaging [23-25,77]. However, other features, including upper respiratory tract symptoms, myalgias, diarrhea, and smell or taste disorders, are also common (table 3). Although some clinical features (in particular smell or taste disorders) are more common with COVID-19 than with other viral respiratory infections [80], there are no specific symptoms or signs that can reliably distinguish COVID-19 [81]. However, development of dyspnea approximately one week after the onset of initial symptoms may be suggestive of COVID-19. (See 'Course and complications' below.)
The range of associated symptoms was illustrated in a report of over 370,000 confirmed COVID-19 cases with known symptom status reported to the CDC in the United States [54]:
?Cough in 50 percent
?Fever (subjective or >100.4°F/38°C) in 43 percent
?Myalgia in 36 percent
?Headache in 34 percent
?Dyspnea in 29 percent
?Sore throat in 20 percent
?Diarrhea in 19 percent
?Nausea/vomiting in 12 percent
?Loss of smell or taste, abdominal pain, and rhinorrhea in fewer than 10 percent each
Other cohort studies of patients with confirmed COVID-19 have reported a similar range of clinical findings [23,25,82-84]. Notably, fever is not a universal finding on presentation, even among hospitalized cohorts. In one study, fever was reported in almost all patients, but approximately 20 percent had a very low grade fever <100.4°F/38°C [23]. In another study of 1099 patients from Wuhan and other areas in China, fever (defined as an axillary temperature over 99.5°F/37.5°C) was present in only 44 percent on admission but was ultimately noted in 89 percent during the hospitalization [77]. In a study of over 5000 patients who were hospitalized with COVID-19 in New York, only 31 percent had a temperature >100.4°F/38°C at presentation [29].
In some studies, smell and taste disorders (eg, anosmia and dysgeusia) have been more frequently reported [85-89]. In a meta-analysis of observational studies, the pooled prevalence estimates for smell or taste abnormalities were 52 and 44 percent, respectively (although rates ranged from 5 to 98 percent across studies) [88]. In one survey of 202 outpatients with mild COVID-19 in Italy, 64 percent reported alterations in smell or taste, and 24 percent reported very severe alterations; smell or taste changes were reported as the only symptom in 3 percent overall and preceded symptoms in another 12 percent [90]. However, the rate of objective smell or taste anomalies may be lower than the self-reported rates. In another study, 38 percent of the 86 patients who reported total lack of smell at the time of evaluation had a normal smell function on objective testing [91]. Most subjective smell and taste disorders associated with COVID-19 do not appear to be permanent; in a follow-up survey of the 202 patients in Italy with COVID-19, 89 percent of those who noted smell or taste alterations reported resolution or improvement by four weeks [92].
Although not noted in the majority of patients, gastrointestinal symptoms (eg, nausea and diarrhea) may be the presenting complaint in some patients [23,25,84,93]. In a systematic review of studies reporting on gastrointestinal symptoms in patients with confirmed COVID-19, the pooled prevalence was 18 percent overall, with diarrhea, nausea/vomiting, or abdominal pain reported in 13, 10, and 9 percent, respectively [94].
Conjunctivitis has also been described [95]. Nonspecific signs and symptoms, such as falls, general health decline, and delirium, have been described in older adults, particularly those over 80 years old and those with underlying neurocognitive impairments [96].
Dermatologic findings in patients with COVID-19 are not well characterized. There have been reports of maculopapular, urticarial, and vesicular eruptions and transient livedo reticularis [97-99]. Reddish-purple nodules on the distal digits similar in appearance to pernio (chilblains) have also been described, mainly in children and young adults with documented or suspected COVID-19, although an association has not been clearly established [99-102]. Some are calling this finding "COVID toes." (See "Coronavirus disease 2019 (COVID-19): Cutaneous manifestations and issues related to dermatologic care", section on 'Cutaneous manifestations of COVID-19'.)
Course and complications — As above, symptomatic infection can range from mild to critical. (See 'Spectrum of severity and case fatality rates' above.)
Some patients with initially nonsevere symptoms may progress over the course of a week. In one study of 138 patients hospitalized in Wuhan for pneumonia due to SARS-CoV-2, dyspnea developed after a median of five days since the onset of symptoms, and hospital admission occurred after a median of seven days of symptoms [25]. In another study, the median time to dyspnea was eight days [23].
Several complications of COVID-19 have been described:
?Respiratory failure – Acute respiratory distress syndrome (ARDS) is the major complication in patients with severe disease and can manifest shortly after the onset of dyspnea. In the study of 138 patients described above, ARDS developed in 20 percent a median of eight days after the onset of symptoms; mechanical ventilation was implemented in 12.3 percent [25]. In large studies from the United States, 12 to 24 percent of hospitalized patients have required mechanical ventilation [29,32]. (See "Coronavirus disease 2019 (COVID-19): Critical care and airway management issues", section on 'Clinical features in critically ill patients'.)
?Cardiac and cardiovascular complications – Other complications have included arrhythmias, acute cardiac injury, and shock [25,55,103,104]. In one study, these were reported in 17, 7, and 9 percent, respectively [25]. In a series of 21 severely ill patients admitted to the ICU in the United States, one-third developed cardiomyopathy [103]. (See "Coronavirus disease 2019 (COVID-19): Myocardial injury", section on 'Clinical features' and "Coronavirus disease 2019 (COVID-19): Arrhythmias and conduction system disease", section on 'Clinical manifestations'.)
?Thromboembolic complications – Thromboembolic complications, including pulmonary embolism and acute stroke (even in patients younger than 50 years of age without risk factors), have also been reported [105-111]. (See "Coronavirus disease 2019 (COVID-19): Hypercoagulability", section on 'Clinical features' and "Coronavirus disease 2019 (COVID-19): Neurologic complications and management of neurologic conditions", section on 'Cerebrovascular disease'.)
?Inflammatory complications – Some patients with severe COVID-19 have laboratory evidence of an exuberant inflammatory response, similar to cytokine release syndrome, with persistent fevers, elevated inflammatory markers (eg, D-dimer, ferritin), and elevated proinflammatory cytokines; these laboratory abnormalities have been associated with critical and fatal illnesses [23,112,113]. (See 'Risk factors for severe illness' above.)
Other inflammatory complications and auto-antibody-mediated manifestations have been described [114,115]. Guillain-Barré syndrome may occur, with onset 5 to 10 days after initial symptoms [116]. A multisystem inflammatory syndrome with clinical features similar to those of Kawasaki disease and toxic shock syndrome has also been described in children with COVID-19 (table 4); this syndrome has been rarely reported in adults as well [117-119]. These are discussed in detail elsewhere. (See "Coronavirus disease 2019 (COVID-19): Neurologic complications and management of neurologic conditions", section on 'Guillain-Barré syndrome' and "Coronavirus disease 2019 (COVID-19): Multisystem inflammatory syndrome in children".)
?Secondary infections – Secondary infections do not appear to be common complications of COVID-19 overall, although data are limited [120,121]. In a review of nine studies, mainly from China, the reported rate of bacterial or fungal coinfections was 8 percent (in 62 of 806); these included mainly respiratory infections and bacteremia [120]. Several reports have described presumptive invasive aspergillosis among immunocompetent patients with ARDS from COVID-19, although the frequency of this complication is uncertain [122-125]. In one prospective study of 108 patients on mechanical ventilation for COVID-19 in Italy, probable aspergillosis was diagnosed in 30 (28 percent) based on elevated serum or bronchoalveolar lavage (BAL) galactomannan levels, growth of aspergillus on BAL cultures, or a cavitary infiltrate without other cause [125].
Autopsy studies have noted detectable SARS-CoV-2 RNA (and, in some cases, antigen) in the kidneys, liver, heart, brain, and blood in addition to respiratory tract specimens, suggesting that the virus disseminates systemically in some cases; whether direct viral cytopathic effects at these sites contribute to the complications observed is uncertain [126-129].
Recovery and long-term sequelae — According to the WHO, recovery time appears to be around two weeks for mild infections and three to six weeks for severe disease based on early data from China [130]. However, the recovery course is variable and depends on age and pre-existing comorbidities in addition to illness severity.
In a survey of 350 patients with COVID-19 in the United States, only 39 percent of those who had been hospitalized reported a return to baseline health by 14 to 21 days after diagnosis [131]. Similarly, in a study of 143 patients who had been hospitalized for COVID-19 in Italy (of whom seven had been mechanically ventilated), only 13 percent were symptom free after a mean of 60 days following disease onset [132]. The most common persistent symptoms were fatigue (53 percent), dyspnea (43 percent), joint pain (27 percent), and chest pain (22 percent); none had fever or features concerning for acute illness. However, persistent severe illness with weeks of fever and pneumonia associated with underlying immunosuppression has been reported [133].
Patients with milder initial infections also frequently have prolonged symptoms [131,134]. In a survey of 292 patients diagnosed with COVID-19 in the outpatient setting, only 65 percent reported a return to baseline health by 14 to 21 days after diagnosis [134]. Those who did return to baseline health did so a median of 7 days after diagnosis. Symptoms that were most likely to persist beyond 14 to 21 days included cough (43 percent) and fatigue (35 percent); fever and chills persisted in only 3 and 4 percent. Although a lack of return to baseline health was associated with older age and a greater number of underlying comorbidities, approximately one in five individuals aged 18 to 34 years who were previously healthy reported that they did not return to baseline within two to three weeks.
Systematic evaluation of the long-term sequelae of COVID-19 is lacking, but emerging data [135-137] and evidence from other coronaviruses [138] suggest the potential for ongoing respiratory impairment. Moreover, a cardiac imaging study suggested the potential for cardiac sequelae after COVID-19, even among patients managed in the outpatient setting [139]. Patients who were critically ill with COVID-19 may also be at risk for post-intensive care syndrome (persistent impairments in cognition, mental health, and/or physical function following survival of critical illness), although the incidence following COVID-19 is unknown. (See "Coronavirus disease 2019 (COVID-19): Critical care and airway management issues", section on 'Long term sequelae' and "Post-intensive care syndrome (PICS)".)
Some patients who have recovered from COVID-19 have persistently or recurrently positive nucleic acid amplification tests (NAATs) for SARS-CoV-2. Although recurrent infection or reinfection cannot be definitively ruled out in these settings, evidence suggests that these are unlikely. This is discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Epidemiology, virology, and prevention", section on 'Immunity and risk of reinfection'.)
LABORATORY FINDINGS
Common laboratory findings among hospitalized patients with COVID-19 include lymphopenia, elevated aminotransaminase levels, elevated lactate dehydrogenase levels, elevated inflammatory markers (eg, ferritin, C-reactive protein, and erythrocyte sedimentation rate), and abnormalities in coagulation tests [25,77,84].
Lymphopenia is especially common, even though the total white blood cell count can vary [23-25,140]. As an example, in a series of 393 adult patients hospitalized with COVID-19 in New York City, 90 percent had a lymphocyte count <1500/microL; leukocytosis (>10,000/microL) and leukopenia (<4000/microL) were each reported in approximately 15 percent [84].
On admission, many patients with pneumonia have normal serum procalcitonin levels; however, in those requiring ICU care, they are more likely to be elevated [23-25].
Several laboratory features, including high D-dimer levels and more severe lymphopenia, have been associated with critical illness or mortality [24]. These are discussed elsewhere. (See 'Risk factors for severe illness' above.)
Abnormalities in coagulation testing are also discussed in detail elsewhere. (See "Coronavirus disease 2019 (COVID-19): Hypercoagulability", section on 'Coagulation abnormalities'.)
IMAGING FINDINGS
Chest radiographs — Chest radiographs may be normal in early or mild disease. In a retrospective study of 64 patients in Hong Kong with documented COVID-19, 20 percent did not have any abnormalities on chest radiograph at any point during the illness [141]. Common abnormal radiograph findings were consolidation and ground glass opacities, with bilateral, peripheral, and lower lung zone distributions; lung involvement increased over the course of illness, with a peak in severity at 10 to 12 days after symptom onset.
Chest CT — Although chest computed tomography (CT) may be more sensitive than chest radiograph and some chest CT findings may be characteristic of COVID-19, no finding can completely rule in or rule out the possibility of COVID-19. In the United States, the American College of Radiology (ACR) recommends not using chest CT for screening or diagnosis of COVID-19 and recommends reserving it for hospitalized patients when needed for management [142]. If CT is performed, the Radiological Society of North America has categorized features as typical, indeterminate, or atypical for COVID-19, and has suggested corresponding language for the interpretation report (table 5) [143].
Chest CT in patients with COVID-19 most commonly demonstrates ground-glass opacification with or without consolidative abnormalities, consistent with viral pneumonia [83,144]. As an example, in a systematic review of studies evaluating the chest CT findings in over 2700 patients with COVID-19, the following abnormalities were noted [145]:
?Ground-glass opacifications – 83 percent
?Ground-glass opacifications with mixed consolidation – 58 percent
?Adjacent pleural thickening – 52 percent
?Interlobular septal thickening – 48 percent
?Air bronchograms – 46 percent
Other less common findings were a crazy paving pattern (ground-glass opacifications with superimposed septal thickening), bronchiectasis, pleural effusion, pericardial effusion, and lymphadenopathy.
Chest CT abnormalities in COVID-19 are often bilateral, have a peripheral distribution, and involve the lower lobes.
Although these findings are common in COVID-19, they are not unique to it. In a study of 1014 patients in Wuhan who underwent both RT-PCR testing and chest CT for evaluation of COVID-19, a "positive" chest CT for COVID-19 (as determined by a consensus of two radiologists) had a sensitivity of 97 percent, using the PCR tests as a reference; however, specificity was only 25 percent [146]. The low specificity may be related to other etiologies causing similar CT findings. In another study comparing chest CTs from 219 patients with COVID-19 in China and 205 patients with other causes of viral pneumonia in the United States, COVID-19 cases were more likely to have a peripheral distribution (80 versus 57 percent), ground-glass opacities (91 versus 68 percent), fine reticular opacities (56 versus 22 percent), vascular thickening (59 versus 22 percent), and reverse halo sign (11 versus 1 percent), but less likely to have a central and peripheral distribution (14 versus 35 percent), air bronchogram (14 versus 23 percent), pleural thickening (15 versus 33 percent), pleural effusion (4 versus 39 percent), and lymphadenopathy (2.7 versus 10 percent) [147].
As with chest radiographs, chest CT may be normal soon after the onset of symptoms, with abnormalities more likely to develop over the course of illness [82,148]. However, chest CT abnormalities have also been identified in patients prior to the development of symptoms and even prior to the detection of viral RNA from upper respiratory specimens [83,149].
Among patients who clinically improve, resolution of radiographic abnormalities may lag behind improvements in fever and hypoxia [150].
SPECIAL POPULATIONS
Pregnant and breastfeeding women — The general approach to prevention, evaluation, diagnosis, and treatment of pregnant women with suspected COVID-19 is largely similar to that in nonpregnant individuals. Issues specific to pregnant and breastfeeding women are discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Pregnancy issues".)
Children — Symptomatic infection in children appears to be relatively uncommon; when it occurs, it is usually mild, although severe cases have been reported [72-75]. Details of COVID-19 in children are discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Clinical manifestations and diagnosis in children".)
People with HIV — The impact of HIV infection on the natural history of COVID-19 is uncertain. The clinical features appear the same as in the general population. Small cohort studies have also suggested that outcomes in patients with HIV are largely similar to those seen in the general population [151-153], although HIV infection has been associated with more severe COVID-19 in some observational studies [154]. As an example, in a multicenter cohort study from Spain, the age-and sex-adjusted mortality rate of patients with HIV and COVID-19 was 3.7 per 10,000 people compared with 2.1 per 10,000 for the general Spanish population [154]. However, many of the comorbid conditions associated with severe COVID-19 (eg, cardiovascular disease) occur frequently among persons with HIV [155], and it is unclear whether these or other potential confounding features, rather than HIV infection itself, contribute to the risk. Baseline viral load or CD4 cell count was not associated with worse COVID-19 outcomes among patients with HIV infection in a small study, although most patients in that study had virologic suppression and CD4 cell counts >200 cells/microL [156].
Issues specific to the management of patients with HIV and COVID-19 are discussed elsewhere. (See "Coronavirus disease 2019 (COVID-19): Management in hospitalized adults", section on 'People with HIV'.)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Coronavirus disease 2019 (COVID-19) – International public health and government guidelines" and "Society guideline links: Coronavirus disease 2019 (COVID-19) – Guidelines for specialty care" and "Society guideline links: Coronavirus disease 2019 (COVID-19) – Resources for patients".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
?Basics topics (see "Patient education: Coronavirus disease 2019 (COVID-19) overview (The Basics)" and "Patient education: Coronavirus disease 2019 (COVID-19) and pregnancy (The Basics)" and "Patient education: Coronavirus disease 2019 (COVID-19) and children (The Basics)")
SUMMARY AND RECOMMENDATIONS
?In late 2019, a novel coronavirus, now designated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was identified as the cause of an outbreak of acute respiratory illness in Wuhan, a city in China. In February 2020, the World Health Organization (WHO) designated the disease COVID-19, which stands for coronavirus disease 2019. (See 'Introduction' above.)
?The incubation period for COVID-19 may be as long as 14 days, with most cases occurring four to five days after exposure. Pneumonia is the most frequent serious manifestation of infection, with approximately 15 percent of patients developing severe infection with hypoxia, dyspnea, or extensive pulmonary involvement. (See 'Incubation period' above and 'Clinical manifestations' above.)
?In addition to fever, cough, and/or dyspnea, other features, including upper respiratory tract symptoms, myalgias, diarrhea, and loss of senses of smell or taste, are also common (table 3). There are no specific clinical features that can yet reliably distinguish COVID-19 from other viral respiratory infections, although development of dyspnea several days after the onset of initial symptoms is suggestive of COVID-19. (See 'Initial presentation' above.)
?Acute respiratory distress syndrome (ARDS) is the major complication in patients with severe disease and can manifest shortly after the onset of dyspnea. Many other complications have been reported, including thromboembolic events, acute cardiac injury, kidney injury, and inflammatory complications. (See 'Course and complications' above and "Coronavirus disease 2019 (COVID-19): Critical care and airway management issues", section on 'Clinical features in critically ill patients' and "Coronavirus disease 2019 (COVID-19): Hypercoagulability" and "Coronavirus disease 2019 (COVID-19): Myocardial injury" and "Coronavirus disease 2019 (COVID-19): Multisystem inflammatory syndrome in children".)
?Individuals of any age can acquire SARS-CoV-2 infection, although adults of middle age and older are most commonly affected, and older adults are more likely to have severe disease. Other features associated with severe illness include medical comorbidities (table 1) and specific laboratory abnormalities (table 2). (See 'Spectrum of severity and case fatality rates' above.)
?The possibility of COVID-19 should be considered primarily in patients with compatible symptoms (table 3), in particular fever and/or respiratory tract symptoms, who reside in or have traveled to areas with community transmission or who have had recent close contact with a confirmed or suspected case of COVID-19. Clinicians should also be aware of the possibility of COVID-19 in patients with severe respiratory illness when no other etiology can be identified. If possible, all symptomatic patients with suspected SARS-CoV-2 infection should undergo testing. Testing for and diagnosis of COVID-19 are discussed in detail elsewhere. (See "Coronavirus disease 2019 (COVID-19): Diagnosis", section on 'Diagnostic approach'.)
?Upon suspicion of COVID-19, infection control measures should be implemented. Infection control in the home and in health care settings is discussed in detail elsewhere. (See "Coronavirus disease 2019 (COVID-19): Infection control in health care and home settings", section on 'Infection control in the health care setting'.)
?Interim guidance has been issued by the WHO and by the United States Centers for Disease Control and Prevention (CDC), as well as other expert organizations. These are updated on an ongoing basis. Links to these guidelines can be found elsewhere. (See 'Society guideline links' above.)
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I take CME and I am fully licensed and double board certified.
CME is not research.
If i see on average of 10 covid 19 patients a day and most of them have respiratory issues, bilateral pneumonia, hypoxia, including ARDS on ventilators, and only few of them have myocarditis then based on my clinical experience respiratory system is the number one covid 19 target, and not the heart. I personally saw at least 200 Covid patients so far. That’s plenty of clinical experience.
Btw, by research you and the original poster mean “googling it”. That is not research. Please stick with nonmedical topics or go to medical school. Google school of medicine does not count.
I have been seeing/trewting at least 10 hospitalized covid patients a day. Do you really think i need to do research?
No. From my own experience,
Covid predominately attacks the lungs. Myocarditis is not that frequent.
Yes. Many
Ok. Call amarin on Monday and tell them to edit their website and edit TV commercial where they specifically say “increased risk of bleeding”. They probably made a mistake. (Sarcasm :).
I work at trauma hospital and have been seeing trauma patients every day, many of them with brain hemorrhages.
Vascepa decreases platelet activity and that maybe one of the mechanisms for beneficial cardiovascular effects in Reduce It trial.
However, if you fall and hit your head, most likely you will not develop brain bleed. The fact that she did, may be due to Vascepa’ s antiplatelet effects.
From Amarin website
Bleeding. Serious bleeding can happen in people who take VASCEPA. Your risk of bleeding may increase if you are also taking a blood thinner medicine.
Yes is that why Amarin TV commercial states “increased bleeding risk”. Call them to remove it. They probably made a mistake.
Yes is that way Amarin TV commercial states “increased bleeding risk”. Call them to remove it. They probably made a mistake.
Embolic stroke was lower
Hope you recover quickly. I would stop Vacsepa for a month.
It probably helped to propagate the bleed. Vascepa is stopped before dental and other surgeries. It has antiplatelet activity.
So the answer to your question is the opposite of your gut feeling.
Thanks a lot
Everybody is well.
Will see. Looks promising