Abstract Book Vol. 2 [International Conference on AIDS (14th: 2002: Barcelona, Spain)]

XIV International AIDS Conference

Abstracts WeOrC1375-WeOrC1378 95

WeOrC1375 Malaria infection elevates HIV-1 viral load
J.G. Kublin1, C.S. Jere2, W.C. Miller3, I.F. Hoffman3, N. Chimbiya2, T.E. Taylor4,
M.E. Molyneux5. University of Maryland School of Medicine, 1 Caryl Lane,
Philadelphia, PA, 19118, United States; 2College of Medicine, Blantyre, Malawi;
3University of North Carolina, Chapel Hill, United States; 4Michigan State
University, East Lansing, United States; 5Malawi-Liverpool-Wellcome Trust
Research Programme, Blantyre, Malawi
Background: HIV infection increases malaria parasitemia and incidence of
malarial fevers, and in one case-control study the mean HIV-1 viral load was
higher in adults with malaria than in others. To assess the impact of malaria on
HIV infection, we conducted a prospective cohort study in rural Malawi.
Methods: We screened, identified and recruited HIV-1-positive adults (N=362)
into the cohort. Participants were seen at routine visits every 2 months, at interim visits for any illness, and on designated days after each therapy for malaria.
History, physical exam and blood-film microscopy were performed. We compared
HIV-1 RNA levels (log) at the baseline visit to levels at the first visit positive for
malaria parasitemia.
Results: 161 HIV positive participants experienced at least one episode of R falciparum parasitemia. Persons with parasitemia at baseline (N=32) or within the
first 28 days after enrollment (N=10) were excluded from the HIV-1 RNA analysis.
Among the remaining 119 persons, HIV RNA levels were available at baseline
and during parasitemia for 73 persons. The mean RNA was 343757 copies/ml
at the baseline visit and 500772/ml at the first episode of parasitemia. The mean
paired (parasitemia - baseline) difference in RNA levels was 0.25 log (p = 0.0005).
Among persons with subjective or measured fever and parasitemia, the difference
was slightly greater, 0.35 log (p = 0.0003). The time to a parasitemia episode
(mean = 89 days; median 75 days) did not correlate with the difference in HIV-1
RNA.
Conclusions: HIV RNA levels were significantly increased over baseline among
persons with malaria. We are now studying viral loads in these individuals over
several months after their malaria episode, and comparing the profiles with persons having no malaria. A malaria-associated increase in viral load, especially if
sustained, could lead to increased transmission of HIV and more rapid disease
progression, and thus have substantial public health implications.
Presenting author: James Kublin, 1 Caryl Lane, Philadelphia, PA, 19118, United
States, Tel.: [phone], Fax: [phone], E-mail: jameskublin
@ merck.com
WeOrC1 376 Schistosomiasis and HIV in co-infected individuals
- egg excretion
P. Kallestrup', E. Gomo2, R. Zinyama2, B.K. Pedersen1, B.J. Vennervald3,
A.E. Butterworth4, H. Ullum1. 1Department of Clinical Immunology
Rigshospitalet, 8 Glen Carron Avenue, Highlands, Harare, Denmark; 2Blair
Research Institute, Harare, Zimbabwe; 3Danish Bilharziosis Institute,
Copenhagen, Denmark; 4Biomedical Research and Training Institute, Harare,
Zimbabwe
Background: One objective of our ongoing study "Influence of Schistosomiasis Infection on Viral Replication, Disease Progression and Immune Activation
in HIV+ Individuals" is to describe the interaction between immune function as
expressed by CD4 count and S. haematobium (Sh) egg excretion in co-infected
and HIV- controls. A negative association between HIV and Sh egg excretion has
been suggested. The dependence on CD4 T cells for growth, maturation and egg
excretion of schistosomiasis parasites has been demonstrated in mice(Science
2001, 294(5545):1358-1361).
Methods: The randomised, controlled study is being conducted in Madziwa Area,
Mashonaland Central Province of Zimbabwe. HIV status, CD4 count and number
of eosinophils are determined by standard methods. Sh ova are obtained using
the syringe urine filtration technique on three consecutive urine samples. 76 coinfected and 64 Sh+ HIV- participants have been included. Data are presented
as means and quartiles and were analyzed by Mann-Whitney ranksum test and
Spearmann correlation.
Results: CD4 count was higher in the HIV-group(778, 605-1081 cells/pL) than
in the HIV+group(326, 166-588 cells/kL, P<0.001). Mean number of Sh eggs
excreted in urine did not differ between the groups(HIV+:3.5, 0.6-13.2; HIV-:3,3,
1,0-12,5;P=0,5). Futhermore did Sh eggs not correlate to CD4 count in any of the
two groups(HIV+:Rs=0,05; HIV-:Rs=-0.12). A weak positive correlation between
Sh eggs and eosinophils was observed in the HIV-group(Rs=0,28; P<0,05) but
not in the HIV+ group(Rs=0,006).
Conclusions: The present study cannot confirm previous reports of lower excretion of Sh eggs in HIV+ individuals. We do not find defective excretion of Sh eggs
in individuals with low CD4 counts. Lack of difference in egg excretion between
HIV- and HIV+ participants demonstrates that low Sh egg excretion with low CD4
counts is not a universal phenomenon.
Presenting author: Per Kallestrup, 8 Glen Carron Avenue, Highlands, Harare,
Zimbabwe, Tel.: [phone], Fax: [phone], E-mail: kallestrup@dadl
net.dk

WeOrCi1377 1Visceral Leishmaniasis: A comparative study of
patients with and without Human
Immunodeficiency Virus infection
C.F.V. Takeda1, L.A. Cartaxo1, G.A. Ponte1, A.P Sa1, J.R. Mesquita1,
R.P. Oliveira Jr.2. Hospital S&o Jos6 de Doengas Infecciosas/ Secretaria de
Sadde do Estado do Ceard, Rua Senador Machado, 181, Ap. 2003, Mucuripe,
60165-170, Fortaleza, Brazil; 2Hospital S&o Jos6 de Doengas
Infecciosas/Secretaria de Sadde do Estado do Ceard, Fortaleza, Brazil
Background: Visceral leishmaniasis (VL) is a worldwide disseminated protozoal
infection, endemic in Brazil, associated with considerable morbidity For the last
twenty years it has been reported as a common complication of patients infected
with human immunodeficiency virus (HIV) mainly in the Mediterranean area. The
clinical presentation and outcome of VL in HIV-infected patients are not well
known and few comparative studies have been done. This study also highlights
the increasing incidence of HIV-VL coinfection in Brazil due to the spread of HIV
to rural areas and the VL to suburban areas.
Method: We retrospectively studied the characteristics of VL in patients with and
without HIV infection, between 1995-2001, performed in a referral hospital in the
Northeast of Brazil.We used Fisher exact test in all those cell values less than 5.
Results: It was diagnosed 75 episodes of VL in 69 patients. Eleven (15.95%)
were coinfected, 75% of them had AIDS, and the mean CD4+ lymphocytes count
was 146.47/mm3. The mean age at diagnosis was higher in HIV-infected patients
(32.54 versus 20.98 yr), and the ratio male/female was similar in both groups.
The bone marrow aspirate was positive in 78.9% non coinfected versus 90.9%
coinfected patients. Clinical and laboratory data were similar to patients non
HIV- infected, except for the lower frequency of splenomegaly (p=0,0000275)
and higher relapse rate (p=0.0031). Mortality was higher in the HIV-infected
group(p=0.000227). Five deaths in the HIV-infected group were directly attributed
to VL.
Conclusions: There were no major differences in clinical manifestations or laboratory data between the two groups. Mortality and relapses are more common in
HIV patients. This coinfection behaves as opportunistic infection, usually affecting
HIV- infected patients with severe immunodepression.
Presenting author: Christianne Takeda, Rua Senador Machado, 181, Ap. 2003,
Mucuripe, 60165-170, Fortaleza, Brazil, Tel.: [phone], Fax: [phone],
E-mail: [email protected]
WeOrC 378 Hepatitis G virus (HGV) infection does not prolong
survival of patients with early-stage HIV disease:
importance of baseline HIV viral load as a
predictor of mortality
D. Brust1, S. Jagannatha1, B. Herpin1, K. Miller1, J. Metcalf1, D. Lau2, H. Alter1,
H.C. Lane1, J. Falloon1, A. Fauci1. 1NIH, NIH/NIAID, 3011 Edgewood Road,
Kensington, MD, United States; 2University of Texas, Galveston, United States
Background: Two recent studies reported that HGV infection improved the outcome of HIV disease; however, neither study evaluated baseline HIV viral load,
a known predictor of outcome. To address this issue, we analyzed the impact
of HGV infection on survival in a cohort originally enrolled in an HIV treatment
protocol from 1988-91.
Methods: 180 subjects with early disease (CD4 counts > 500 cells/mm3 and no
history of Ols) were equally randomized to receive either daily zidovudine (ZDV),
interferon (INF), or ZDV and INF to assess the impact of these regimens on HIV.
At study end, subjects continued to follow-up. Baseline HIV viral load and HGV
RNA were performed on frozen samples. Subject survival was determined by
chart review and a Death Index database search. To determine the impact of
HGV status on survival, a Kaplan-Meier (KM) analysis and a Cox proportional
hazards model (which accounted for such variables as CD4 count, HIV viral load
and treatment arm) were performed.
Results: 37% of the cohort was HGV infected. Baseline HIV viral load and CD4
count were not different between HGV-positive and negative subjects. Median
follow-up was 9.6 years. At study termination, 49% of patients were alive, 27%
dead, and 24% lost-to-follow-up. A KM analysis indicated that HGV co-infected
participants had increased mortality when compared to HGV-negative subjects
(p = 0.036). However, when other factors associated with HIV survival were accounted for, the only robust predictor of survival was baseline HIV viral load (p =
0.008).
Conclusions: In this study, HGV co-infection tended to worsen, rather than improve, mortality. Our analysis underscores the importance of including baseline
HIV viral load when modeling survival. Additionally, our results suggest that the
proposed protective effect of HGV co-infection may not be universally applicable
to all HIV-infected people, and in particular, may be linked to disease stage.
Presenting author: Douglas Brust, NIH/NIAID, 3011 Edgewood Road, Kensington, MD, United States, Tel.: [phone], Fax: [phone], E-mail:
dbrust@ niaid.nih.gov