The Bunyaviridae are a very large family of single-strand, enveloped RNA viruses (more than 300 viruses) and consists of five genera of viruses: Orthobunyavirus, Phlebovirus, Nairovirus, Hantavirus, and Tospovirus (Tospoviruses infect only plants). They are found in and transmitted by arthropods (e.g. mosquitoes, ticks, sand flies) and rodents, and can occasionally infect humans. Several viruses of the Bunyaviridae virus family can produce mild to severe disease in human, in animals, and sometimes in both. This is the base for the requirements of handling some of these viruses in high containment (Biosafety Level 3 or even Biosafety level 4).
This opens up an entire new avenue: Alphaviruses, which constitute a genus of more than 30 viruses in the Togaviridae family, are lipid-enveloped, positive-sense RNA viruses.
All human pathogenic alphaviruses are mosquito borne.
Epidemiology • The presence of infected mosquitoes is required for disease outbreak. Human-to-human transmission does not occur.
New World alphaviruses include Eastern, Western, and Venezuelan equine encephalitis viruses (EEEV, WEEV, and VEEV, respectively), which are found in North and South America. Old World alphaviruses, especially chikungunya (CHIK), Sindbis, Ross River, and O'nyong-nyong viruses, found in Europe, Africa, and Asia, cause a fever, arthralgia, and rash syndrome.
In most cases, except for CHIK virus, the life cycle of the viruses requires mosquitoes and an animal host in nature, other than humans.
Pathogenesis • Alphaviruses enter cells by receptor-mediated endocytosis and exit by budding from the plasma membrane.
Alphaviruses enter the body via mosquito bites and replicate in various tissues, including Langerhans cells, which then migrate to lymph nodes, causing viremia. Viremia results in invasion of the central nervous system (CNS) by alphaviruses that cause encephalitis or of the joints and internal organs by viruses that cause fever, arthralgia, and rash. All alphaviruses suppress the innate immune response by inhibiting JAK/STAT signaling, a major early determinant of disease severity.
At later times, recovery is mediated by virus-neutralizing antibodies and cytotoxic T cells. In the CNS, virus replication in neurons is suppressed indefinitely by antibody-secreting B cells.
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