Jazz, what jumped out to me in SK's answer to MM's Immunity question on 3-13-06 was the portion highlighted below:
Mike M., Ladenburg: Re: long-term immunity, have we found that occurs with any other viruses than Lassa? SK: “So far I believe that’s been the only model we’ve looked at in regard to long-term immunity or at least the only one we’ve presented any data on. That will be an important part of the MOA as we move fwd, and we will incorporating that in our studies for diseases such as HIV & Influenza as we move fwd.”
“…OR AT LEAST THE ONLY ONE WE’VE PRESENTED ANY DATA ON.”
"In order to fully evaluate the potential of bavituximab in HIV therapy, we have expanded our collaborations in the HIV area. Our current collaborators include investigators at Tulane National Primate Research Center, Duke University, as well as contract research laboratories.
Some of our collaborators at Duke University recently received funding from the Gates Foundation for studies related to their HIV Vaccine Initiative. As part of these studies, we will be working with these researchers to assess phospholpids as a potential target for combatting HIV.
Because the program is being conducteds by the researchers at Duke, we are not able to discuss the details at this time, but needless to say, we are very pleased to be involved in this collaboration, in increasing recognition that phospholipids may be an attractive target in HIV infection.
We will provide an update on these studies as mutually agreed upon with our collaborators or at appropriate times for data generated internally, or at contract research institutions."
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Here's a bit of that increasing recognition that phospholipids may be an attractive target in HIV infection.-
this first interesting snip is quite recent- Aug 2, 2006
HIV, the etiological agent of AIDS, has the capability of selectively infecting and ultimately incapacitating the immune system. The progressive depletion of CD4 and CD8 T cells, one of the hallmarks of HIV-1 infection, is caused in part by a general increase in apoptosis of infected and uninfected T cells [15]. HIV also targets macrophages and alters their production of inflammatory cytokines [16, 17], expression of surface re- ceptors [18], and phagocytic function [19 –21], thus crippling key innate immune functions. Given the documented increase in the incidence of apoptosis during HIV infection, it is probable that these dying cells and features associated with apoptosis might create a microenvironment that influences HIV infection and replication [22]. Consistent with this hypothesis, it has been demonstrated that HIV-infected cells, as well as the HIV virions, have PS exposed on their surface and that PS is a cofactor for establishing HIV infection in monocytic cells [23, 24]. The PS expressed on HIV virions and/or the PS expressed on monocytes/macrophages are functional, as PS inhibitors are able to reduce HIV infection of U937 monocytic cells and monocyte-derived macrophages (MDM)
Phosphatidylserine on HIV Envelope Is a Cofactor for Infection of Monocytic Cells1
HIV-1 is an enveloped retrovirus that acquires its outer membrane as the virion exits the cell. Because of the association of apoptosis with the progression of AIDS, HIV-1-infected T cells or macrophages might be expected to express elevated levels of surface phosphatidylserine (PS), a hallmark of programmed cell death. Virions produced by these cells would also be predicted to have PS on the surface of their envelopes. In this study, data are presented that support this hypothesis and suggest that PS is required for macrophage infection. The PS-specific protein annexin V was used to enrich for virus particles and to inhibit HIV-1 replication in primary macrophages, but not T cells. HIV-1 replication was also significantly inhibited with vesicles consisting of PS, but not phosphatidylcholine. PS is specifically required for HIV-1 infection because viruses pseudotyped with vesicular stomatitis virus G and amphotropic murine leukemia virus envelopes were not inhibited by PS vesicles or annexin V. These data indicate that PS is an important cofactor for HIV-1 infection of macrophages.
Secretory Leukocyte Protease Inhibitor Binds to Annexin II, a Cofactor for Macrophage HIV-1 Infection
".....Persistent evidence favors the existence of additional cofactors for binding and/or entry of HIV-1, including components of the host cell membrane acquired during viral budding (13). Among these host-derived constituents in the viral envelope is the phospholipid, phosphatidylserine (PS; reference 14), which predicts a potential interactive molecule on the receptive host cell that may facilitate virus binding, entry, and/or fusion.".....
also- early evidence of a natural/native anti-phosphatidylserine having an effect
Antiphosphatidylserine Antibodies in Human Immunodeficiency Virus-l+ Patients Correlate With Evidence of T-cell Apoptosis and Mediate Antibody-Dependent Cellular Cytotoxicity
...."Significant levels of IgG to CL, PS, or both were observed in 23 patients lacking evidence of thrombophilic events or any peculiar clinical feature of HIV-1 infection."
..." these antibodies greatly improved the effector functions of autologous macrophages in antibodydependent cellular cytotoxicity (ADCC) assays...."
..."Because PS is exteriorized by apoptotic lymphocytes, its persistence may stimulate antibodies which cooperate with macrophages in the clearance of dead cells by an enhanced ADCC mechanism. "
"Our study focuses on the significance of autoantibodies to phospholipid antigens during HIV-I infection. By using a panel of antigenic specificities, including both anionic and neutral phospholipids, we identified CL andor PS as the predominant targets of those molecules in about 12% of HIV-l' patients...
"...target CEM cells coated with increasing amounts of purified anti-PS IgG from 4 HIV-1' subjects greatly enhanced the ADCC function in these macrophages. This increment of cytolytic properties was remarkable in tests using macrophages in combination with autologous anti-PS IgG..."
"...We believe this is the first observation on the functional role of antiphospholipid reactivities in HIV-l infection...."
the only human data reported to date- (from the HCV clinical trial)
..." After a single dose of bavituximab, among patients treated with the higher 1mg/kg and 3mg/kg dose levels, 50% achieved a greater than 75% (0.6 log) reduction in serum HCV RNA with a maximum 97% (1.5 log) reduction. These patients had an average reduction in serum HCV RNA levels of 0.8 log during the course of the 12-week follow-up period. Signs of anti-viral activity were seen at all dose levels including the initial dose of 0.1mg/kg. Even at this low dose, one-third of patients experienced a greater than 75% (0.6 log) reduction in serum HCV RNA levels.
Bavituximab also showed signs of durable anti-viral activity after a single dose, with some subjects achieving a greater than 80% (0.7 log) reduction in viral load by day four and maintaining a greater than 60% reduction in serum HCV levels up through the end of the study at week 12..."
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