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HIV-1 expression in chimpanzees can be activated by CD8+ cell depletion or CMV infection
B A Castro1, J Homsy, E Lennette
1Cancer Research Institute, University of California, San Francisco 94143-0128.
Insights
CD8+ T-cells suppress HIV replication in vivo. Introducing cytomegalovirus (CMV) reactivated HIV in infected chimpanzees, suggesting viral co-infections impact HIV progression.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- CD8+ T-cells play a crucial role in controlling viral infections.
- Human Immunodeficiency Virus (HIV) infection is a chronic condition with complex disease progression.
- Cytomegalovirus (CMV) is a common viral infection that can remain latent.
Purpose of the Study:
- To investigate the in vivo role of CD8+ T-cell antiviral activity in controlling HIV-1 replication.
- To determine if cytomegalovirus (CMV) acts as a cofactor influencing HIV-1 infection outcomes.
- To evaluate the impact of CD8+ cell depletion and CMV co-infection on HIV-1 replication in chimpanzees.
Main Methods:
- Depletion of CD8+ T-cells in HIV-1 infected chimpanzees using anti-CD8 monoclonal antibodies.
- Inoculation of HIV-1 infected chimpanzees with cytomegalovirus (CMV)-infected fibroblasts.
- Monitoring of HIV-1 viral load in CD4+ lymphocytes before and after experimental interventions.
Main Results:
- CD8+ cell depletion led to the recovery of HIV-1 from CD4+ lymphocytes in treated chimpanzees.
- HIV-1 viral load increased in chimpanzees inoculated with CMV-infected fibroblasts.
- These changes were observed in animals where HIV-1 was previously undetectable or rarely detected.
Conclusions:
- CD8+ T-cell mediated suppression is a significant factor in controlling HIV-1 replication in vivo.
- Co-infection with cytomegalovirus (CMV) can potentially increase HIV-1 replication.
- These findings suggest that viral co-infections and immune status are critical cofactors in HIV-1 pathogenesis.
Abstract:
CD8+ cell antiviral activity and cytomegalovirus (CMV) were investigated in vivo as possible cofactors influencing the outcome of HIV-1 infection. The role of CD8+ cell suppression of HIV replication was evaluated by depleting CD8+ cells in two infected chimpanzees by inoculation with monoclonal anti-CD8 antibodies. Two other infected animals were injected with chimpanzee CMV (CCMV)-infected human fibroblasts to determine if exposure to this virus would induce HIV replication. Treatment with anti-CD8 antibody resulted in recovery of virus from the CD4+ lymphocytes of one animal at 1, 4, and 6 months, and from a second animal at 1 month postinoculation. In contrast, virus had been recovered only once or not at all from these infected chimpanzees for 4 years prior to treatment. Similarly, HIV was recovered from the CD4+ cells of the two animals 2 to 3 months after inoculation of CCMV-infected fibroblasts but not after inoculation of control uninfected fibroblasts. These studies suggest that CD8+ cell-mediated suppression and the presence of other viruses (such as CMV) could act as cofactors in influencing the extent of HIV-1 replication in vivo and, possibly, progression to disease.
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