Abstract
BACKGROUND:
Africa bears the burden of approximately 7001 seroconversion on the speed of HIV-1 disease progression, as measured by the outcome CD4+ T-cell (CD4) counts textless350 cells/μL and/or death. We hypothesized that people who had been infected with Schistosoma spp. at the time they acquired HIV-1 infection would have impaired antiviral immune response, thus leading them to progress twice as fast to a CD4 count less than 350 cells/μL or death than would people who had been free of schistosomes at time of HIV-1 seroconversion.
METHODS AND PRINCIPAL FINDINGS:
We conducted a longitudinal study in Tanzania from 2006 to 2017 using stored blood spot samples, demographic surveillance and sero-survey data from the community, and a review of clinical charts. A competing risk analysis was performed to look at the difference in time to reaching CD4 counts textless 350 cells/μL and/or death in HIV-1-infected people who were infected versus not infected with Schistosoma spp. at time of HIV-1 seroconversion. We found an 82subHazard Ratio = 0.18[0.068,0.50], p = 0.001) after adjusting for age, occupation, clinic attendance and time-dependent covariates.
CONCLUSIONS:
Our study demonstrates that people with schistosome infection at the time of HIV-seroconversion develop adverse HIV outcomes more slowly than those without. The findings are contrary to our original hypothesis. Our current longitudinal findings suggest complex interactions between HIV-1 and schistosome co-infections that may be modulated over time. We urge new immunological studies to investigate the long-term impact of schistosome infection on HIV-1 viral load and CD4 counts as well as related immunologic pathways.
Africa bears the burden of approximately 7001 seroconversion on the speed of HIV-1 disease progression, as measured by the outcome CD4+ T-cell (CD4) counts textless350 cells/μL and/or death. We hypothesized that people who had been infected with Schistosoma spp. at the time they acquired HIV-1 infection would have impaired antiviral immune response, thus leading them to progress twice as fast to a CD4 count less than 350 cells/μL or death than would people who had been free of schistosomes at time of HIV-1 seroconversion.
METHODS AND PRINCIPAL FINDINGS:
We conducted a longitudinal study in Tanzania from 2006 to 2017 using stored blood spot samples, demographic surveillance and sero-survey data from the community, and a review of clinical charts. A competing risk analysis was performed to look at the difference in time to reaching CD4 counts textless 350 cells/μL and/or death in HIV-1-infected people who were infected versus not infected with Schistosoma spp. at time of HIV-1 seroconversion. We found an 82subHazard Ratio = 0.18[0.068,0.50], p = 0.001) after adjusting for age, occupation, clinic attendance and time-dependent covariates.
CONCLUSIONS:
Our study demonstrates that people with schistosome infection at the time of HIV-seroconversion develop adverse HIV outcomes more slowly than those without. The findings are contrary to our original hypothesis. Our current longitudinal findings suggest complex interactions between HIV-1 and schistosome co-infections that may be modulated over time. We urge new immunological studies to investigate the long-term impact of schistosome infection on HIV-1 viral load and CD4 counts as well as related immunologic pathways.
| Original language | English |
|---|---|
| Article number | e0006613 |
| Journal | PLoS Neglected Tropical Diseases |
| Volume | 12 |
| Issue number | 7 |
| ISSN | 1935-2727 |
| DOIs | |
| Publication status | Published - 1-Jul-2018 |
| Externally published | Yes |
Keywords
- Acquired Immunodeficiency Syndrome
- Adult
- Animals
- CD4 Lymphocyte Count
- Coinfection
- Female
- HIV Infections
- HIV-1
- Humans
- Longitudinal Studies
- Male
- Middle Aged
- Schistosoma
- Schistosomiasis
- Tanzania