Georgia D Tomaras1, Barton F Haynes. 1. Duke Human Vaccine Institute, Duke University Medical Center, Durham, NC 27710, USA. gdt@duke.edu
Abstract
PURPOSE OF REVIEW: The humoral immune response to HIV-1 throughout infection is comprised of complex mixtures of antibody isotypes with numerous HIV-1 specificities. However, unlike antibody responses to most infections, protective antibody responses are delayed and do not arise until long after HIV-1 latency is established. We review recent data on HIV-1-specific antibody isotypes induced following HIV-1 transmission: to understand the effects of HIV-1 on B cell and T cell effector responses, to understand the timing of the rise and fall of different anti-HIV-1 antibodies and to understand how antibodies could contribute to protective immunity if they were either pre-existing or elicited immediately after HIV-1 transmission. RECENT FINDINGS: Studies of the earliest events following infection by the transmitted/founder virus have recently revealed that early destruction of B cell generative microenvironments may be responsible for delay of potentially protective anti-HIV-1 antibody responses. Unlike the initial CD8 T cell response to HIV-1, the initial induced antibody response is usually ineffective in controlling virus replication during acute HIV-1 infection. SUMMARY: The antibody isotypes and specificities elicited during HIV-1 infection can provide a window into deciphering the detrimental effects of HIV-1 on B cell and T cell responses. Additionally, further characterization of the virus inhibitory capabilities of anti-HIV-1 antibody isotypes can define the spectrum of potential protective HIV-1 antibodies that could be readily elicited by experimental vaccines and adjuvants.
PURPOSE OF REVIEW: The humoral immune response to HIV-1 throughout infection is comprised of complex mixtures of antibody isotypes with numerous HIV-1 specificities. However, unlike antibody responses to most infections, protective antibody responses are delayed and do not arise until long after HIV-1 latency is established. We review recent data on HIV-1-specific antibody isotypes induced following HIV-1 transmission: to understand the effects of HIV-1 on B cell and T cell effector responses, to understand the timing of the rise and fall of different anti-HIV-1 antibodies and to understand how antibodies could contribute to protective immunity if they were either pre-existing or elicited immediately after HIV-1 transmission. RECENT FINDINGS: Studies of the earliest events following infection by the transmitted/founder virus have recently revealed that early destruction of B cell generative microenvironments may be responsible for delay of potentially protective anti-HIV-1 antibody responses. Unlike the initial CD8 T cell response to HIV-1, the initial induced antibody response is usually ineffective in controlling virus replication during acute HIV-1 infection. SUMMARY: The antibody isotypes and specificities elicited during HIV-1 infection can provide a window into deciphering the detrimental effects of HIV-1 on B cell and T cell responses. Additionally, further characterization of the virus inhibitory capabilities of anti-HIV-1 antibody isotypes can define the spectrum of potential protective HIV-1 antibodies that could be readily elicited by experimental vaccines and adjuvants.
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