B-cell subset alterations and correlated factors in HIV-1 infection

Pensieroso, Simone; Galli, Laura; Nozza, Silvia; Ruffin, Nicolas; Castagna, Antonella; Tambussi, Giuseppe; Hejdeman, Bo; Misciagna, D.; Riva, Agostino; Malnati, Mauro S.; Chiodi, Francesca; Scarlatti, Gabriella

doi:10.1097/qad.0b013e32835edc47

Cited by 76 publications

(98 citation statements)

References 27 publications

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“…Although effective HAART is regarded to have no effect on RM, some restoration may be feasible upon HAART initiation especially in primary infection [13,16], triggering their increase, which is in line with our results were treated patients had higher levels of RM B cells compared to naïve. In our study increase of RM levels in both groups may be attributed to vaccination.…”

Section: Discussionsupporting

confidence: 90%

“…Our study encourages the identification and quantification of certain B cell subsets involved in T cell independent responses, confirming few other authors claiming that, not only IgM and ITS memory B cells, but also on RM and AM, may contribute to impaired protection against encapsulated bacteria [12,[16][17][18]. Recent studies focus on B cell memory and immunological response against polysaccharide vaccine, though most constitute solely cross-sectional studies [12].…”

Section: Discussionsupporting

confidence: 79%

“…The loss of memory is reflected in the decline of antigen specific memory B cells post vaccination, which is not reconstituted by HAART [14][15][16]. RM cells are maintained if HAART is initiated early post-primary HIV infection [16].…”

Section: Introductionmentioning

confidence: 99%

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Alterations in memory B cell subsets upon immunization against Streptococcus pneumoniae in HIV-1 infected adults

et al. 2015

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 79%

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Alterations in memory B cell subsets upon immunization against Streptococcus pneumoniae in HIV-1 infected adults

et al. 2015

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“…48 However, even potent treatments are not able to fully revert the loss of memory B cells and their function during chronic infection at the level observed in healthy individuals. 38,46,[49][50][51] Aging of the innate immune compartment…”

Section: 31mentioning

confidence: 99%

Assessing immune aging in HIV-infected patients

Appay

Sauce

2016

Virulence

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Many of the alterations that affect innate and adaptive immune cell compartments in HIV-infected patients are reminiscent of the process of immune aging, characteristic of old age. These alterations define the immunological age of individuals and are likely to participate to the decline of immune competence with HIV disease progression. It is therefore important to characterize these changes, which point toward the accumulation of highly differentiated immunocompetent cells, associated with overall telomere length shortening, as well as understanding their etiology, especially related to the impact of chronic immune activation. Particular attention should be given to the exhaustion of primary immune resources, including haematopoietic progenitors and na€ ıve cells, which holds the key for effective hematopoiesis and immune response induction, respectively. The alteration of these compartments during HIV infection certainly represents the foundation of the immune parallel with aging.

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“…Early initiation of ART in adults and children, however, is associated with improved memory B-cell functions [29,37]. The defect, once established in chronic infection, may not be corrected even through a long period of treatment [39].…”

Section: Redistribution Of Classic and Rare Populations Of Memory B Cmentioning

confidence: 99%

Impairment of B-cell functions during HIV-1 infection

Amu

Ruffin

Réthi

et al. 2013

Aids

Self Cite

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A variety of B-cell dysfunctions are manifested during HIV-1 infection, as reported early during the HIV-1 epidemic. It is not unusual that the pathogenic mechanisms presented to elucidate impairment of B-cell responses during HIV-1 infection focus on the impact of reduced T-cell numbers and functions, and lack of germinal center formation in lymphoid tissues. To our understanding, however, perturbation of B-cell phenotype and function during HIV-1 infection may begin at several different B-cell developmental stages. These impairments can be mediated by intrinsic B-cell defects as well as by the lack of proper T-cell help. In this review, we will highlight some of the pathways and molecular interactions leading to B-cell impairment prior to germinal center formation and B-cell activation mediated through the B-cell receptor in response to HIV-1 antigens. Recent studies indicate a regulatory role for B cells on T-cell biology and immune responses. We will discuss some of these novel findings and how these regulatory mechanisms could potentially be affected by the intrinsic defects of B cells taking place during HIV-1 infection.

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B-cell subset alterations and correlated factors in HIV-1 infection

Abstract: Our results indicate that viremia and nadir CD4 T cells are important prognostic markers of B-cell perturbations and provide evidence that resting memory B-cell depletion during chronic infection is not reverted upon successful antiretroviral therapy.

Cited by 76 publications

References 27 publications

Alterations in memory B cell subsets upon immunization against Streptococcus pneumoniae in HIV-1 infected adults

Alterations in memory B cell subsets upon immunization against Streptococcus pneumoniae in HIV-1 infected adults

Assessing immune aging in HIV-infected patients

Impairment of B-cell functions during HIV-1 infection

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