Abstract

BackgroundWhile initiation of highly active antiretroviral therapy (HAART) during primary HIV-1 infection occasionally results in transient control of viral replication after treatment interruption, the vast majority of patients eventually experience a rebound in plasma viremia.ResultsHere we report a case of a patient who was started on HAART during symptomatic primary infection and who has subsequently maintained viral loads of < 50 copies/mL for more than nine years after the cessation of treatment. This patient had a high baseline viral load and has maintained a relatively high frequency of latently infected CD4+ T cells. In addition, he does not have any known protective HLA alleles. Thus it is unlikely that he was destined to become a natural elite controller or suppressor. The mechanism of control of viral replication is unclear; he is infected with a CCR5/CXCR4 dual-tropic virus that is fully replication-competent in vitro. In addition, his spouse, who transmitted the virus to him, developed AIDS. The patient's CD4+ T cells are fully susceptible to HIV-1 infection, and he has low titers of neutralizing antibodies to heterologous and autologous HIV-1 isolates. Furthermore, his CD8+ T cells do not have potent HIV suppressive activity.ConclusionThis report suggests that some patients may be capable of controlling pathogenic HIV-1 isolates for extended periods of time after the cessation of HAART through a mechanism that is distinct from the potent cytotoxic T lymphocyte (CTL) mediated suppression that has been reported in many elite suppressors.

Highlights

  • While initiation of highly active antiretroviral therapy (HAART) during primary HIV-1 infection occasionally results in transient control of viral replication after treatment interruption, the vast majority of patients eventually experience a rebound in plasma viremia

  • We present a case of a patient infected with a replication-competent, dual-tropic HIV-1 isolate who was started on treatment during primary infection

  • Acute Infection and Early Disease Research Program (AIEDRP) study and started on a regimen of zidovudine, lamivudine, and indinavir within 48 hours of admission. This regimen was changed to abacavir, lamivudine and efavirenz at week four and by week 16, his viral load was < 50 copies/ml. He stopped taking his antiretrovirals at week 36 for a 2 week period, and his viral load rebounded to 22,000 copies/ml

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Summary

Introduction

While initiation of highly active antiretroviral therapy (HAART) during primary HIV-1 infection occasionally results in transient control of viral replication after treatment interruption, the vast majority of patients eventually experience a rebound in plasma viremia. The mechanisms involved in elite control are not fully understood, but some ES appear to be infected with fully replication-competent virus [2,3,4,5] that continues to It is not clear whether it will be possible to elicit similar levels of immune control in patients with progressive HIV-1 disease. Five of thirtytwo patients treated during primary HIV-1 infection maintained control of viral replication for more than six months after treatment was interrupted [23] While this phenomenon is not routinely seen with early treatment [24,25,26], these cases strongly suggest that the immune system can be manipulated to control HIV-1 replication in some patients. This could be the basis for the design of a successful therapeutic vaccine

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