Open Access Highly Accessed Research article

High levels of T lymphocyte activation in Leishmania-HIV-1 co-infected individuals despite low HIV viral load

Joanna R Santos-Oliveira1, Carmem BW Giacoia-Gripp2, Priscilla Alexandrino de Oliveira3, Valdir S Amato4, Jose Ângelo L Lindoso5, Hiro Goto5, Manoel P Oliveira-Neto6, Marise S Mattos6, Beatriz Grinsztejn6, Mariza G Morgado2 and Alda M Da-Cruz1*

Author Affiliations

1 Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz -FIOCRUZ. Av. Brasil 4365. Rio de Janeiro, CEP 21040-360, Brazil

2 Laboratório de Aids e Imunologia Molecular; Instituto Oswaldo Cruz - FIOCRUZ, Av. Brasil 4365. Rio de Janeiro, CEP 21040-360, Brazil

3 Hospital-Dia Profa. Esterina Corsini, Hospital Universitário, Universidade Federal de Mato Grosso do Sul (UFMS). Mato Grosso do Sul, CEP 79070-900, Brazil

4 Serviço de Doenças Infecciosas e Parasitárias, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil. CEP 05403-010, São Paulo, Brazil

5 Instituto de Medicina Tropical de São Paulo - Universidade de São Paulo, São Paulo, CEP 05403-010, Brazil

6 Instituto de Pesquisa Clínica Evandro Chagas, IPEC - FIOCRUZ, Av. Brasil 4365. Rio de Janeiro, CEP 21040-360, Brazil

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BMC Infectious Diseases 2010, 10:358  doi:10.1186/1471-2334-10-358

Published: 20 December 2010



Concomitant infections may influence HIV progression by causing chronic activation leading to decline in T-cell function. In the Americas, visceral (AVL) and tegumentary leishmaniasis (ATL) have emerged as important opportunistic infections in HIV-AIDS patients and both of those diseases have been implicated as potentially important co-factors in disease progression. We investigated whether leishmaniasis increases lymphocyte activation in HIV-1 co-infected patients. This might contribute to impaired cellular immune function.


To address this issue we analyzed CD4+ T absolute counts and the proportion of CD8+ T cells expressing CD38 in Leishmania/HIV co-infected patients that recovered after anti-leishmanial therapy.


We found that, despite clinical remission of leishmaniasis, AVL co-infected patients presented a more severe immunossupression as suggested by CD4+ T cell counts under 200 cells/mm3, differing from ATL/HIV-AIDS cases that tends to show higher lymphocytes levels (over 350 cells/mm3). Furthermore, five out of nine, AVL/HIV-AIDS presented low CD4+ T cell counts in spite of low or undetectable viral load. Expression of CD38 on CD8+ T lymphocytes was significantly higher in AVL or ATL/HIV-AIDS cases compared to HIV/AIDS patients without leishmaniasis or healthy subjects.


Leishmania infection can increase the degree of immune system activation in individuals concomitantly infected with HIV. In addition, AVL/HIV-AIDS patients can present low CD4+ T cell counts and higher proportion of activated T lymphocytes even when HIV viral load is suppressed under HAART. This fact can cause a misinterpretation of these laboratorial markers in co-infected patients.