Abstract

BackgroundThe risk of postnatal HIV transmission is associated with the magnitude of the milk virus load. While HIV-specific cellular immune responses control systemic virus load and are detectable in milk, the contribution of these responses to the control of virus load in milk is unknown.MethodsWe assessed the magnitude of the immunodominant GagRY11 and subdominant EnvKY9-specific CD8+ T lymphocyte response in blood and milk of 10 A*3002+, HIV-infected Malawian women throughout the period of lactation and correlated this response to milk virus RNA load and markers of breast inflammation.ResultsThe magnitude and kinetics of the HIV-specific CD8+ T lymphocyte responses were discordant in blood and milk of the right and left breast, indicating independent regulation of these responses in each breast. However, there was no correlation between the magnitude of the HIV-specific CD8+ T lymphocyte response and the milk virus RNA load. Further, there was no correlation between the magnitude of this response and markers of breast inflammation.ConclusionsThe magnitude of the HIV-specific CD8+ T lymphocyte response in milk does not appear to be solely determined by the milk virus RNA load and is likely only one of the factors contributing to maintenance of low virus load in milk.

Highlights

  • HIV transmission via breastfeeding remains a major mode of infant HIV acquisition, accounting for nearly half of the 350,000 infant HIV infections occurring annually [1,2]

  • Phenotype of T lymphocytes in milk of HIV-infected and uninfected lactating women

  • The median proportion of CD4+ T lymphocytes in milk was significantly lower in HIV-infected women than uninfected women (17% vs. 52%, p = 0.002)

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Summary

Introduction

HIV transmission via breastfeeding remains a major mode of infant HIV acquisition, accounting for nearly half of the 350,000 infant HIV infections occurring annually [1,2]. In the absence of antiretroviral prophylaxis, only a small minority of HIV-infected mothers transmit the virus via breastfeeding despite chronic low dose virus exposure [2,3,4]. This low rate of virus transmission suggests immune protection of the majority of infants from virus acquisition during breastfeeding. Immune containment of local virus replication in the breast may contribute to protection against virus transmission via breastfeeding. The risk of postnatal HIV transmission is associated with the magnitude of the milk virus load. While HIVspecific cellular immune responses control systemic virus load and are detectable in milk, the contribution of these responses to the control of virus load in milk is unknown

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