HIV-1 Disease Progression and Survival in an Adult Population in Zimbabwe: Is There an Effect of the Mannose Binding Lectin Deficiency?
HIV infection remains a major global health burden since its discovery in 1983. Sub-Saharan Africa is the region hardest hit by the HIV/AIDS pandemic where 63% of the 33 million infected people live. While there is marked person-to-person variability in susceptibility, progression, and survival with HIV infection, there is a paucity of predictive diagnostics associated with these clinical endpoints. In this regard, the deficiency in plasma Mannose Binding Lectin (MBL) is a common opsonic defect reported to increase susceptibility infections, including HIV. To the best of our knowledge, we report here the first study on the putative role of MBL deficiency on HIV progression and survival in an African adult population. We hypothesized that MBL deficiency has a role to play in HIV infection by increasing HIV disease progression and decreasing survival. We assessed the role of MBL deficiency on HIV disease progression and survival in a Zimbabwean adult population enrolled in the Mupfure Schistosomiasis and HIV (MUSH) cohort. We analyzed blood samples for MBL levels, MBL2 genotypes, HIV-1 status, viral load, and CD4(+) T cell counts. Participants were followed for 3 years wherein the endpoints were measured at baseline, 6 weeks, and 3, 6, 12, 24, and 36 months. Disease progression was measured as the rate of decline in CD4(+) T cell counts and the rate of increase in HIV viral load. We assessed 197 HIV positive adults where 83% (164) were women with a median age of 31 years. Prevalence of plasma MBL deficiency (less than 100 μg/L) and MBL2 deficient genetic variants (A/O and O/O genotypes) was 21% (42 out of 197) and 39% (74 out of 190), respectively. We did not observe a significant role to explain individual variation in mortality, change of CD4(+) T cell count, and viral load by MBL plasma deficiency or MBL2 genetic variants from baseline to 3 years follow up period in this adult population. We suggest the need for global OMICS research and that the present findings attest to the large between-population variability in a host of factors that can predispose individuals susceptible to HIV progression and mortality. We therefore cannot recommend at this time the use of plasma MBL levels or MBL2 genetic variants as a prognostic marker in HIV infection, disease progression, and survival in this adult population in Africa.
1 Faculty of Health Sciences, School of Public Health, University of the Witwatersrand , Johannesburg, South Africa .|2 Medical Research Council of Zimbabwe , Ministry of Health and Child Welfare, Harare, Zimbabwe .|3 Letten Research Foundation , Harare, Zimbabwe .
Rutendo B L
RB
Zinyama-Gutsire
1 Faculty of Health Sciences, School of Public Health, University of the Witwatersrand , Johannesburg, South Africa .|13 Epidemiology and Strategic Information Unit, Human Sciences Research Council , Gauteng, South Africa .
Charles
C
Chasela
4 Centre for Global Health, Department of Public Health, Aarhus University , Aarhus, Denmark .
Per
P
Kallestrup
3 Letten Research Foundation , Harare, Zimbabwe .|5 College of Health Sciences, University of Zimbabwe , Harare, Zimbabwe .
Simbarashe
S
Rusakaniko
6 Department of Clinical Biochemistry, Immunology and Genetics, Statens Serum Institute , Copenhagen, Denmark.
Michael
M
Christiansen
3 Letten Research Foundation , Harare, Zimbabwe .
Bernard
B
Ngara
7 Department of Medical Laboratory Sciences, College of Health Sciences, University of Zimbabwe Harare , Zimbabwe .
Exnevia
E
Gomo
8 Laboratory of Molecular Medicine, Copenhagen University , Rigshospitalet, Copenhagen, Denmark .
Henrik
H
Ullum
9 Tissue Typing Laboratory, Department of Clinical Immunology, Copenhagen University , Rigshospitalet, Copenhagen, Denmark .
Christian
C
Erikstrup
9 Tissue Typing Laboratory, Department of Clinical Immunology, Copenhagen University , Rigshospitalet, Copenhagen, Denmark .
Hans O
HO
Madsen
3 Letten Research Foundation , Harare, Zimbabwe .|5 College of Health Sciences, University of Zimbabwe , Harare, Zimbabwe .|10 Division of Women and Children, Rigshospitalet Oslo University Hospital and University of Oslo , Oslo, Norway .
Babill
B
Stray-Pedersen
9 Tissue Typing Laboratory, Department of Clinical Immunology, Copenhagen University , Rigshospitalet, Copenhagen, Denmark .
Peter
P
Garred
12 Department of Laboratory Medicine and Medical Sciences, University of KwaZulu Natal , Durban, South Africa .
Takafira
T
Mduluza
D000328:Adult; D000483:Alleles; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D015658:HIV Infections / Q000235:genetics / Q000378:metabolism / Q000401:mortality* / Q000473:pathology*; D015497:HIV-1; D006239:Haplotypes / Q000235:genetics; D006801:Humans; D008297:Male; D037601:Mannose-Binding Lectin / Q000172:deficiency* / Q000235:genetics; D008661:Metabolism, Inborn Errors / Q000235:genetics / Q000503:physiopathology*; D008875:Middle Aged; D015030:Zimbabwe
D037601:Mannose-Binding Lectin