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Review
. 2011 Apr;23(1):13-8.
doi: 10.1177/0022034511398874.

Virus-host interactions in HIV pathogenesis: directions for therapy

Affiliations
Review

Virus-host interactions in HIV pathogenesis: directions for therapy

J A Levy. Adv Dent Res. 2011 Apr.

Abstract

The challenge of controlling HIV infection involves an understanding of the heterogeneity of the virus, its wide cellular host range, its primary routes of transmission, and the immunologic and intrinsic cellular factors that can prevent its transmission and replication. Identification of HIV-infected individuals who have survived more than 10 years without signs of the infection and without therapy encourages studies examining the natural mechanisms for resistance to infection and disease. Within the immune system, emphasis should be given to the innate or natural response that appears within minutes of the infection and offers the optimal time for controlling HIV. All these parameters in HIV pathogenesis underline the information needed to develop optimal anti-HIV therapies and an effective AIDS vaccine.

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Figures

Fig. 1.
Fig. 1.
Replication of early and late HIV-1 isolates from the same individual. Replication of 2 strains of HIV-1 recovered from the same individual over time. HIV-1SF2 (0), isolated early in the course of infection, replicates slowly and to low titer in the established HUT 78 T-cell line. In contrast, HIV-1SF13 (Δ), recovered when the patient had AIDS, grows rapidly and to high titer in the same cells. These and other biologic differences between these 2 strains have been used to distinguish viruses in culture as non-virulent and virulent strains. Reprinted from Levy (2007) with permission.
Fig. 2.
Fig. 2.
Correlation of PDC number with viral load in acutely infected individuals. Individuals who have been acutely infected with HIV (within the preceding 3 months) were evaluated for viral load as well as PDC number before receiving any therapy. It is evident that those infected individuals with high PDC number had the lowest viral loads.

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