The catch 22 of immune response to AIDs viral infection

A strong antigen-specific T-cell response to HIV infection is important for controlling virus replication; however, because HIV selectively infects and replicates in CD4 T cells, increased number of these cells in response to viral infection may also be detrimental as these cells provide fuel for the infection to grow.

In the March 15 issue of the Journal of Clinical Investigation, Mark Feinberg and colleagues, of Emory University Vaccine Center, analyze the specific parameters of T-cell activation that may be harmful or helpful in fighting HIV infection by looking at simian immunodeficiency viral (SIV) replication in rhesus macaques where they have blocked CD4 and CD8 T-cell co-stimulation pathways.

The study provides clear evidence for an important role in the immune activation level directly affects the initial peak of virus in the blood stream. They further show that the steady-state viral levels in chronic infection are directly related to the generation of a primary immune response.

Evidence in this study also indicates, indirectly, that immunological response may indeed be harmful by providing increased numbers of target cells for infection. The work here presents the first set of data to differentiate between helpful and harmful effects of the immune response to HIV, and may therefore contribute to new strategies for combating this disease.

An accompanying commentary by Bruce Walker (Harvard Medical School) and Steven Deeks (University of California, San Francisco) provides a detailed discussion of the different components of the findings and how these results aid in picking apart this complex interplay between HIV infection and our immune response.