By Flossie Wong-Staal, Robert C. Gallo
This reference describes the most recent advances within the improvement and layout of an HIV preventive vaccine-detailing the pathogenesis and genetic variability of HIV an infection for the development of molecular and healing thoughts to minimize the development and transmission of AIDS. With contributions by way of universally well-known gurus within the box, AIDS Vaccine study discusses
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Additional info for AIDS Vaccine Research
However, in the case of HIV, the host immune system is never able to completely control and eradicate the infection. In fact, in an impressive example of subversion of the immune system, HIV utilizes the activated milieu of lymphoid tissue toward its own replicative advantage. Close contact between immune effector cells as well as high levels of pro-inﬂammatory cytokines are characteristic of the lymphoid tissue microenvironment; these conditions favor viral replication in several ways. Activated CD4ϩ T lymphocytes migrating through lymphoid tissue serve as ideal targets for de novo infection with HIV (142–146).
1984. T-lymphocyte T4 molecule behaves as receptor for human retrovirus LAV. Nature 312:767–768. 4. G. S. R. A. A. Axel. 1986. The T4 gene encodes the AIDS virus receptor and is expressed in the immune system and the brain. Cell 47:333–348. 5. A. Berger. 1995. Fusogenic selectivity of the envelope glycoprotein is a major determinant of human immunodeﬁciency virus type 1 tropism for CD4ϩ T-cell lines vs. primary macrophages. Proc Natl Acad Sci USA 92:9004–9008. 6. C. A. Berger. 1996. Cell type-speciﬁc fusion Immunopathogenesis of HIV Infection 7.
A beneﬁcial role for HIV-speciﬁc CTL is also suggested by their presence in the peripheral blood of individuals who are frequently exposed to HIV yet remain uninfected (217,218) and the depletion of HIV-speciﬁc CTL from lymph nodes of patients with advanced HIV disease (219). Studies in nonhuman primates have demonstrated that monkeys subjected to CD8ϩ Tcell depletion manifest diminished control of plasma viremia during primary SIV infection (220); in addition, CD8ϩ T-cell depletion during the chronic phase of SIV infection leads to a prompt and profound increase in levels of viral replication (220–222).