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Memory B-cell depletion is a feature of HIV-2
infection even in the absence of detectable viremia
Rita Tendeiro
a
, Sofia Fernandes
a
, Russell B. Foxall
a
,
Jose ´ M. Marcelino
b,c
, Nuno Taveira
b,d
, Rui S. Soares
a
,
Anto ´ nio P. Baptista
a
, Rita Cavaleiro
a
, Perpe ´tua Gomes
d,e,f
,
Rui M.M. Victorino
a,g
and Ana E. Sousa
a
Objective: Memory B-cell loss has long been recognized as an important contributor to
HIV immunodeficiency. HIV-2 infection, which is characterized by a slow rate of
progression to AIDS and reduced to undetectable viremia, provides a unique model to
investigate B-cell disturbances.
Design and methods: B-cell subsets were evaluated in 38 HIV-2-infected individuals,
along with markers of T-cell activation and serum levels of immunoglobulins and a
major B-cell homeostatic cytokine, B-cell activating factor (BAFF). Untreated HIV-1-
infected and seronegative control individuals were studied in parallel. Statistical
analysis was performed using Mann–Whitney tests and Spearman’s correlations.
Results: We found that HIV-2 was associated with significant depletion of both
unswitched (CD27
þ
IgD
þ
) and switched (CD27
þ
IgD
neg
) memory B-cells that directly
correlated with T-cell activation, even in individuals with undetectable plasma viral
load. Nevertheless, the presence of detectable viremia, even at low levels, was
associated with significant memory B-cell loss and higher BAFF levels. Moreover,
these alterations were not recovered by antiretroviral-therapy, as treated HIV-2-infected
patients showed more pronounced B-cell disturbances, possibly related to their
extended length of infection.
Conclusion: These first data regarding B-cell imbalances during HIV-2 infection show
that, irrespective of viremia, prolonged HIV infection leads to irreversible damage of
memory B-cell homeostasis. ß 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
AIDS 2012, 26:1607–1617
Keywords: AIDS, B-cell activating factor, B-cells, HIV-2, immune activation,
memory B-cells
Introduction
HIV-1 infection is associated with progressive impair-
ment of specific humoral responses and loss of memory
B-cells that are only partly recovered by antiretroviral
therapy (ART) [1–4]. These B-cell disturbances have
been linked to the persistent heightened state of immune
activation associated with HIV-1 infection [3–5]. In fact,
a
Unidade de Imunologia Clı ´nica, Instituto de Medicina Molecular, Faculdade de Medicina,
b
Unidade de Retrovı ´rus e Infecc ¸o ˜es
Associadas, Centro de Patoge ´nese Molecular, Faculdade de Farma ´cia, Universidade de Lisboa,
c
Unidade de Microbiologia
Me ´ dica, Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, Lisboa,
d
Centro de Investigac ¸a ˜ o Interdisciplinar
Egas Moniz (CiiEM), Instituto Superior de Cie ˆ ncias da Sau ´ de Egas Moniz, Caparica,
e
Laborato ´ rio de Biologia Molecular, Servic ¸o de
Medicina Transfusional, Centro Hospitalar Lisboa Ocidental, Hospital Egas Moniz,
f
Centro de Mala ´ria e Doenc ¸as Tropicais,
Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, and
g
Clı ´nica Universita ´ria de Medicina 2, Centro
Hospitalar Lisboa Norte, Hospital Universita ´rio de Santa Maria, Lisboa, Portugal.
Correspondence to Ana E. Sousa, MD, PhD, Unidade de Imunologia Clı ´nica, Instituto de Medicina Molecular, Faculdade de
Medicina, Universidade de Lisboa, Av. Professor Egas Moniz, 1649-028 Lisboa, Portugal.
Tel: +351 21 799 95 25; fax: +351 21 799 95 27; e-mail: asousa@fm.ul.pt
Received: 23 February 2012; revised: 23 May 2012; accepted: 1 June 2012.
DOI:10.1097/QAD.0b013e3283568849
ISSN 0269-9370 Q 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
1607