Hiv One Evolution And Disease Progression Biology Essay


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HIV-1 is notable for its vast ability to evolve as a result of its error-prone reverse transcriptase and high rate of virus production(Lippincott Williams & Wilkins 2009).Within-host HIV-1 evolution is characterized by diversification of the infecting virus population throughout the course of infection. In addition to genetic drift and purifying selection, HIV-1 can evolve under positive selection from antibodies and cytotoxic to what extent virus evolution and escape from immune pressure contribute to HIV-1 disease progression (Lippincott Williams & Wilkins 2009).HIV-1 evolution is most commonly evaluated by measuring viral diversity and divergence in nucleotide sequences(Shankarappa et al.1999) It described a consistent pattern of increasing virus diversity and divergence throughout infection, which was temporally associated with progression to AIDS.


HIV-1 evolution and disease progression markers were evaluated over approximately 5 years of infection among 37 Kenyan women from a prospective, seroincident cohort. Evolution was measured in two genes, gag and env, which are primary targets of cellular and humoral immune responses, respectively. An understanding of the genetics of HIV provides a context for understanding the short- and long-term impact of the same on the physiology of the human body in terms of the pathogenesis of HIV disease, and associated cofactors that

eventually produce AIDS.


The relationship between HIV-1 evolution and disease progression remains particularly unclear with respect to an important component of HIV-1 evolution, evasion of the adaptive immune response.

The primary goal of this study was to evaluate the relationship between HIV-1 evolution and disease progression and to compare this relationship in two different genes, gag and env.

Because these genes are primary targets of different arms of the immune response, immune evasion was also evaluated in relation to virus evolution.


HIV-1 gag and env diversity and divergence were highly correlated in early and late infection. Divergence in gag was strongly correlated with viral load, largely because of the accumulation of synonymous changes. Mutation in gag cytotoxic T-lymphocyte epitopes was associated with higher viral load. There was evidence for adaptive evolution in env, but the extent of env evolution was only weakly associated with neutralizing antibody breadth. Strong correlations between HIV-1 evolution in these two genes as well as across these two times in infection. there was a high correlation between gag diversity and env diversity at both time points as well as between gag divergence and env divergence. Furthermore, within each gene, there was a high correlation between measures of evolution in early and chronic infection. Thus, individuals who had a high diversity in early infection continued to have a high diversity in chronic infection as well as high divergence.


HIV may continue to be virulent because of its fast mutation rate, recombinogenic effect, and its use of human defenses to replicate itself. For instance, superinfection by viruses of different lineages has the potential for generating recombinant viruses with considerable genetic complexity. Such recombination could occur in humans to produce, for example, HIV-3 because biological mechanisms that usually constrain the evolution of viruses may not apply to HIV. That is, HIV may be evolutionarily free of constraints that could reduce its virulence.

While researchers continually develop new drugs to attack the virus, HIV continually produces new variants that are already standing by to circumvent the drug. In addition, replacement of susceptible strains can occur rapidly (Wei et al 1995), and drug-resistant strains can be transmitted producing “primary” resistance in newly infected individuals (Erice et al 1993, Siegrist et al 1994). Therefore, immune system and drug-related selection may broaden the clinical expression of HIV to include uncommon infections and constitutional diseases. Eventually, surveillance of drug-resistant HIV strains may be necessary, similar to surveillance of drug-resistant gonorrhea, malaria, and tuberculosis (Hu et al 1996).



Lippincott Williams & Wilkins results indicate that HIV-1 evolution in gag and env is highly correlated but exhibits gene-specific differences. The different immune pressures on these genesmay partly explain differences in evolution and consequences for HIV-1 disease progression.

Lippincott Williams & Wilkins is the first to directly compare longitudinal relationships between HIV-1 evolution in two genes, immune evasion, and disease progression. Our results support a model in which HIV-1 gag and env evolve in a concerted manner, largely because of similar rates of synonymous evolution. However, because these genes are the primary targets of different adaptive immune responses, gene-specific evolution also occurs. Adaptive evolution in gag is relatively rare but may promote disease progression via CTL escape, whereas adaptive evolution in env is common and may reflect escape from NAb but does not significantly affect viral load. Further longitudinal studies are needed to more clearly elucidate the selective forces acting on env, including autologous NAb. Ultimately, a furtther research for a better understanding of how HIV-1 evolves in response to immune pressure, and how this contributes to disease progression, will provide insight into achieving immune-mediated control of HIV-1 infection.

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