Primary HIV-1 infection sets the stage for important B lymphocyte dysfunctions

Abstract

B cell dysfunctions found in chronic HIV-1 infection appear during PHI and initiation of antiretroviral therapy early during infection may help to preserve the B cell compartment.

Timing of HAART defines the integrity of memory B cells and the longevity of humoral responses in HIV-1 vertically-infected children

“…Antiretroviral therapy permits only partial restoration of the memory B cell compartment (4). In adults, most beneficial effects are obtained when therapy is applied during primary HIV-1 infection (PHI) (22). Perinatal HIV-1 infection is acquired in the milieu of a developing immune system and consequently, in the absence of antiretroviral treatment, PHI in children results in higher levels of HIV-1 viremia compared with adults (28).…”

The inhibitory collagen receptor LAIR-1 (CD305)

“…In one case report from a boy with chronic active EBV infection, decreased expression of LAIR-1 on NK cells was found [48]. In chronic and primary HIV-1 infection, down-regulated expression of LAIR-1 on B cells was interpreted as a sign of hyperactivation [49,50].…”

Two overrepresented B cell populations in HIV-infected individuals undergo apoptosis by different mechanisms

“…Among B cells, a large number of these defects have been associated with HIV-induced immune activation, as evidenced by hypergammaglobulinemia, increased expression of B cell activation markers, decreased responsiveness to B cell stimuli, and increased susceptibility to oncogenesis (1)(2)(3). Several studies have demonstrated that after reduction of HIV plasma viremia by antiretroviral therapy, B cell abnormalities subside, especially those thought to be directly or indirectly associated with virus-induced aberrant immune activation (4)(5)(6). We have demonstrated previously both in longitudinal and cross-sectional analyses that overrepresentation of a distinct B cell population, defined by reduced expression of CD21 and increased secretion of immunoglobulins (7), is likely to be responsible for several of the B cell defects that have been associated with ongoing HIV replication (8)(9)(10).…”