HIV-1 antigen-specific and -nonspecific B cell responses are sensitive to combination antiretroviral therapy. Academic Article uri icon

Overview

abstract

  • We studied how combination antiviral therapy affects B cell abnormalities associated with HIV-1 infection, namely elevated circulating immunoglobulin (Ig)G antibody-secreting cell (ASC) frequencies and hypergammaglobulinemia. Within a few weeks of starting antiviral therapy, there is a marked decline in IgG-ASC frequency in both acutely and chronically infected people, whereas the hypergammaglobulinemia often present during chronic infection is more gradually resolved. These reductions are sustained while HIV-1 replication is suppressed. HIV-1 antigen-specific B cell responses are also affected by therapy, manifested by a rapid decline in circulating gp120-specific ASCs. Anti-gp120 titers slowly decrease in chronically infected individuals and usually fail to mature in acutely infected individuals who were promptly treated with antiretroviral therapy. Long-term nonprogressors have high titer antibody responses to HIV-1 antigens, but no detectable gp120-specific IgG-ASC, and normal (or subnormal) levels of total circulating IgG-ASC. Overall, we conclude that HIV-1 infection drives B cell hyperactivity, and that this polyclonal activation is rapidly responsive to decreases in viral replication caused by combination antiviral therapy.

publication date

  • July 20, 1998

Research

keywords

  • Antiviral Agents
  • B-Lymphocytes
  • HIV Antibodies
  • HIV Antigens
  • HIV Infections
  • HIV-1

Identity

PubMed Central ID

  • PMC2212446

Scopus Document Identifier

  • 0031875614

Digital Object Identifier (DOI)

  • 10.1084/jem.188.2.233

PubMed ID

  • 9670036

Additional Document Info

volume

  • 188

issue

  • 2