The prevalence, incidence and risk factors of herpes simplex virus type 2 infection among pregnant Zimbabwean women followed up nine months after childbirth

Background Herpes simplex virus type 2 (HSV-2) is the leading cause of genital ulcer disease worldwide. The virus can be transmitted to neonates and there are scarce data regarding incidence of HSV-2 among women in pregnancy and after childbirth. The aim of this study is to measure the incidence and risk factors for HSV-2 infection in women followed for 9 months after childbirth. Methods Pregnant women were consecutively enrolled late in pregnancy and followed at six weeks, four and nine months after childbirth. Stored samples were tested for HSV-2 at baseline and again at nine months after childbirth and HSV-2 seropositive samples at nine months after childbirth (seroconverters) were tested retrospectively to identify the seroconversion point. Results One hundred and seventy-three (50.9%) of the 340 consecutively enrolled pregnant women were HSV-2 seronegative at baseline. HSV-2 incidence rate during the 10 months follow up was 9.7 (95% CI 5.4-14.4)/100 and 18.8 (95% CI 13.9-26.1)/100 person years at risk (PYAR) at four months and nine months after childbirth respectively. Analysis restricted to women reporting sexual activity yielded higher incidence rates. The prevalence of HSV-2 amongst the HIV-1 seropositive was 89.3%. Risk factors associated with HSV-2 seropositivity were having other sexual partners in past 12 months (Prevalence Risk Ratio (PRR) 1.8 (95% CI 1.4-2.4) and presence of Trichomonas vaginalis (PRR 1.7 95% CI 1.4-2.1). Polygamy (Incidence Rate Ratio (IRR) 4.4, 95% CI 1.9-10.6) and young age at sexual debut (IRR 3.6, 95% CI 1.6-8.3) were associated with primary HSV-2 infection during the 10 months follow up. Conclusions Incidence of HSV-2 after childbirth is high and the period between late pregnancy and six weeks after childbirth needs to be targeted for prevention of primary HSV-2 infection to avert possible neonatal infections

Role of Mannose-Binding Lectin Deficiency in HIV-1 and <i>Schistosoma</i> Infections in a Rural Adult Population in Zimbabwe

<div><p>Background</p><p>Polymorphism in the <i>MBL2</i> gene lead to MBL deficiency, which has been shown to increase susceptibility to various bacterial, viral and parasitic infections. We assessed role of MBL deficiency in HIV-1 and schistosoma infections in Zimbabwean adults enrolled in the Mupfure Schistosomiasis and HIV Cohort (MUSH Cohort).</p><p>Methods</p><p>HIV-1, <i>S</i>. <i>haematobium</i> and <i>S</i>. <i>mansoni</i> infections were determined at baseline. Plasma MBL concentration was measured by ELISA and <i>MBL2</i> genotypes determined by PCR. We calculated and compared the proportions of plasma MBL deficiency, <i>MBL2</i> structural variant alleles <i>B</i> (codon 54A>G), <i>C</i> (codon 57A>G), and <i>D</i> (codon 52T>C) as well as <i>MBL2</i> promoter variants <i>-550(H/L)</i>, <i>-221</i>(<i>X/Y)</i> and <i>+4</i>(<i>P/Q)</i> between HIV-1 and schistosoma co-infection and control groups using Chi Square test.</p><p>Results</p><p>We assessed 379 adults, 80% females, median age (IQR) 30 (17–41) years. HIV-1, <i>S</i>. <i>haematobium</i> and <i>S</i>. <i>mansoni</i> prevalence were 26%, 43% and 18% respectively in the MUSH baseline survey. Median (IQR) plasma MBL concentration was 800μg/L (192-1936μg/L). Prevalence of plasma MBL deficiency was 18% with high frequency of the <i>C</i> (codon 57G>A) mutant allele (20%). There was no significant difference in median plasma MBL levels between HIV negative (912μg/L) and HIV positive (688μg/L), p = 0.066. However plasma MBL levels at the assay detection limit of 20μg/L were more frequent among the HIV-1 infected (p = 0.007). <i>S</i>. <i>haematobium</i> and <i>S</i>. <i>mansoni</i> infected participants had significantly higher MBL levels than uninfected. All <i>MBL2</i> variants were not associated with HIV-1 infection but promoter variants <i>LY</i> and <i>LL</i> were significantly associated with <i>S</i>. <i>haematobium</i> infection.</p><p>Conclusion</p><p>Our data indicate high prevalence of MBL deficiency, no evidence of association between MBL deficiency and HIV-1 infection. However, lower plasma MBL levels were protective against both <i>S</i>. <i>haematobium</i> and <i>S</i>. <i>mansoni</i> infections and <i>MBL2</i> promoter and variants <i>LY</i> and <i>LL</i> increased susceptibility to <i>S</i>. <i>haematobium</i> infection.</p></div

Distribution of participants between <i>MBL2</i> promoter region haplotypes according to HIV and <i>S</i>. <i>haematobium</i> co-infection status.

<p>This analysis was done using the Chi Square or Fisher’s exact tests, n = 284</p><p>Distribution of participants between <i>MBL2</i> promoter region haplotypes according to HIV and <i>S</i>. <i>haematobium</i> co-infection status.</p

Distribution of participants between <i>MBL2</i> genotypes and promoter region haplotypes according to schistosoma infection status.

<p>This analysis was done using the Fisher’s exact tests, n = 344</p><p>Distribution of participants between <i>MBL2</i> genotypes and promoter region haplotypes according to schistosoma infection status.</p

Distribution of participants between three plasma MBL levels, participants stratified according HIV, <i>S</i>. <i>haematobium</i> and <i>S</i>. <i>mansoni</i> infection and co-infection status.

<p>Prevalence of MBL deficiency, plasma MBL concentration was categorised into normal (above 500μg/L), intermediate (100μg/L- 500μg/L) and deficient (below 100μg/L), analysed by the Chi Square or Fisher’s exact tests, n = 378.</p><p>Distribution of participants between three plasma MBL levels, participants stratified according HIV, <i>S</i>. <i>haematobium</i> and <i>S</i>. <i>mansoni</i> infection and co-infection status.</p

Gene, promoter alleles and haplotype frequencies obtained for <i>MBL2</i> polymorphism among the enrolled Zimbabwean participants.

<p><i>MBL2</i> gene and allele frequencies obtained by direct gene counting, frequencies expressed as percentages.</p><p>Gene, promoter alleles and haplotype frequencies obtained for <i>MBL2</i> polymorphism among the enrolled Zimbabwean participants.</p