Objective: To investigate whether clearance of Leishmania parasites from ti
ssue aspirate smears in patients with HIV and visceral leishmaniasis (VL) c
o-infection treated with pentavalent antimonials is influenced by initial H
IV viral load and to assess the effect of active VL on HIV viral load and r
eplication in vivo.
Methods: Leishmania parasites were identified in Giemsa-stained smears prep
ared from tissue aspirates. Parasite index was determined by quantifying Le
ishmania donovani bodies in smears. HIV-1 RNA was quantitated by using the
nucleic acid sequence-based amplification technique with a limit of detecti
on of 500 copies/ml. All patients were treated with pentavalent antimonials
at 20 mg pentavalent antimony (Sb-V)/kg daily for a total of 28 days. None
of the patients received specific anti-retroviral therapy.
Results: Seventeen patients (73.9%) showed good initial response to antilei
shmanial treatment and the remaining six (26.1%) had very poor response. Am
ong the good responders, 11 (64.7%) had no demonstrable Leishmania donovani
bodies in post-therapy tissue aspirate smear preparations, and in the rema
ining six (35.3%) their parasite loads were reduced to very low levels. Pat
ients with poor response had persistently high parasite index despite compl
etion of anti-leishmanial chemotherapy. Poor responders had pre-treatment m
edian HIV viral load that was > 160-fold higher than responders to anti-lei
shmanial chemotherapy; [410 000 copies/ml (quartile range, 33 000 - 530 000
) and 2500 copies/ml (quartile range 500 - 297 500), respectively]. Further
more, compared with pre-treatment viral concentrations, patients with good
response showed marked reduction in post- treatment viral load. In contrast
, post-treatment HIV viral concentrations were markedly increased among pat
ients with poor response to anti-leishmanial therapy.
Conclusions: The results suggest that pre-treatment HIV viral load influenc
es response to anti-leishmanial chemotherapy and active VL is associated wi
th increased viral replication in vivo, supporting the notion that dual inf
ection plays an important role in the pathogenesis and disease progression
of either infection. (C) 1999 Lippincott Williams & Wilkins.