The testing of dried blood spots (DBSs) for human immunodeficiency type 1 (HIV-1) proviral DNA by PCR is a technology that has proven to be particularly valuable in diagnosing exposed infants. We implemented this technology for HIV-1 early infant diagnosis (EID) and HIV-1 RNA viral load determination in infants born of HIV-1-seropositive mothers from remote areas in Cameroon. The samples were collected between December 2007 and September 2010. Fourteen thousand seven hundred and sixty-three (14,763) DBS samples from infants born of HIV-positive mothers in 108 sites nationwide were tested for HIV. Of these, 1452 were positive on first PCR analyses (PCR1), giving an overall infection rate of 12.30%. We received only 475 DBS specimen for a second PCR testing (PCR2); out of these, 145 were positive. The median HIV-1 RNA viral load for 169 infant DBS samples tested was 6.85 log copies/ml, with values ranging from 3.37 to 8 log copies/ml. The determination of the viral load on the same DBS as that used for PCR1 allowed us to bypass the PCR2. The viral load values were high and tend to decrease with age but with a weak slope. The high values of viral load among these infants call for early and effective administration of antiretroviral therapy (ART). The findings from this study indicate that the use of DBS provides a powerful tool for perinatal screening programs, improvement on the testing algorithm, and follow-up during treatment, and thus should be scaled up to the entire nation.

Background: Human papillomavirus (HPV) is the leading cause of cervical cancers, causing 270.000 deaths annually worldwide of which 85% occur in developing countries with an increasing risk associated to HIV infection. This study aimed at comparing HPV's positivity and genotype distribution in women according to their HIV status and determinants. Methods: A comparative study was carried out in 2012 at the Chantal BIYA International Reference Centre (CIRCB) among 278 women enrolled consecutively at the General Hospital and the Gynaeco-Obstetric and Paediatric Hospital of the City of Yaoundé. HPV genotyping was performed by real-time PCR, HIV serological screening by serial algorithm, CD4 T cell phenotyping by flow cytometry and HIV viral load by Abbott m2000RT. Statistical analyses were performed using Microsoft Excel 2016 and Graph Pad version 6.0 software; with P < 0.05 considered statistically significant.

Background: Human papillomavirus (HPV) is the leading cause of cervical cancers, causing 270.000 deaths annually worldwide of which 85% occur in developing countries with an increasing risk associated to HIV infection. This study aimed at comparing HPV’s positivity and genotype distribution in women according to their HIV status and determinants. Methods: A comparative study was carried out in 2012 at the Chantal BIYA International Reference Centre (CIRCB) among 278 women enrolled consecutively at the General Hospital and the Gynaeco-Obstetric and Paediatric Hospital of the City of Yaoundé. HPV genotyping was performed by real-time PCR, HIV serological screening by serial algorithm, CD4 T cell phenotyping by flow cytometry and HIV viral load by Abbott m2000RT. Statistical analyses were performed using Microsoft Excel 2016 and Graph Pad version 6.0 software; with P<0.05 considered statistically significant. Results: Globally, mean age was 37 ±3 years; median CD4-count for HIV+ was 414 cells/mm 3 [IQR: 264.75-588] and median viremia was 50 RNA copies/mL [IQR: <40-8288]. Overall HPV rate was 38.49% (107/278); 58.88% for single women vs. others (28.97% married, 2.80% divorced, 9.34% for widows), OR: 2.164; p=0.0319. Following HIV status, HPV rate was 43.48% (80/184) among HIV+ vs. 28.72% (27/94) among HIV- (OR: 1.937; p<0.0142); HPV genotypes among HIV+ vs. HIV- were respectively distributed as follows: genotype 16 (3.75% vs. 0.00%, p=0.57), genotype 18 (3.75% vs. 3.70%, p=1.00), co-infection 16 and others (8.75% vs. 7.40%, p=1.00), co-infection 18 and others (8.75% vs. 11.11%, p=0.71), co-infection 16, 18 and others (2.50% vs. 0.00%, p=1.00) and other genotypes (72.50% vs. 77.78%, p=0.80). Among HIV+ participants, HPV rate following CD4 was 62.88% (61/97) for CD4<500 vs. 35.71% (20/56) for CD4≥500 (OR: 3.05; p=0.0012) while HPV rate following HIV viremia was 42.71% (41/96) with <1000 RNA copies/ml vs. 66.00% (33/50) with >1000 RNA copies/ml (OR= 0.384; p =0.009). Conclusion: In Yaoundé, HPV rate appear to be very high, with higher rates of genotypes other than 16 and 18. In the event of HIV infection, the risk of HPV positivity is two times higher, favoured essentially by immunodeficiency. Thus, HIV-infected women should be closely monitored to prevent the emergence of cervical cancer.

Introduction in order to contribute to the improvement of the management of toxoplasmosis in pregnant women in Cameroon, performance of two techniques commonly used in the diagnosis of toxoplasmosis was evaluated. Methods a total of 541 pregnant women were recruited from seven hospitals in two Regions of Cameroon, of which 63% (341: Batch1) were from health facilities (HF) using a immunochromatographic technique (ICT) as a screening test for toxoplasmosis, and 37% (200: Batch2) from those using an immunoenzymatic technique (IEZ). On each sample, Ig (Immunoglobulin) G (IgG) and IgM were tested by three techniques: a Rapid Diagnostic Test (RDT), an Enzyme Linked Immuno Sorbent Assay (ELISA) and a Vidas Enzyme-linked fluorescent assay taken as reference (VIDAS/ELFA). The results from the health facilities were recorded. Results for the IgG assay, our two laboratory methods were sensitive (96.0% and 97.5%) and specific (64.2% and 59.7%). Their concordance rates with the VIDAS/ELFA reference were above 60% (P<0.001). Moreover, for the IgM assay, the performances of the two methods were equivalent: Se= 18.2%, Sp= 99.4% with a low concordance rate (Kappa = 0.24). Considering the results provided by the selected hospitals, the ELISA used in Batch2 showed similar performances to the two techniques used in reference lab while the performances were low for the RDT used in Batch1. Conclusion both methods showed similar performances (good for (IgG) and poor for IgM). However, for the immunochromatographic method, differences in performance were found between our results and those provided by the selected health facilities. These differences suggest a harmonization of diagnostic techniques for toxoplasmosis in pregnant women in Cameroonian health facilities.

Background Cervical cancer, caused by the human papillomavirus (HPV), remains a global health challenge. In HIV highly-burdened settings, it would be relevant to understand the severity of cervical cancer in case of co-infection with HPV. We therefore sought to determine the effect of HPV on the occurrence of cervical lesions among women with versus without HIV-infection. Methods A cross-sectional analytical study was conducted throughout 2012 among 257 women living in Yaoundé, Cameroon. HIV serology, genotyping of high-risk oncogenic HPV and cervical vaginal smear (CVS) were performed for all participants; among those reported to be HIV seropositive, HIV plasma viral load and CD4 count were measured. Results of the CVS were interpreted following the Bethesda 2001 guidelines. Statistical analyses were performed using Graph Pad version 6.0; p < 0.05 was considered statistically significant. Results The mean age of our study participants was 37 ± 6.5 years. According to HIV serology, 184 (71.59%) were HIV-positive vs. 73 (28.40%) HIV-negative women, with a similar age distribution respectively (36 ± 2.80 years versus 42 ± 8.48 years). Among HIV-positive women, median CD4 was 438 [IQR: 317–597] cells/mm3 and median viremia < 40 [IQR: <40 − 2318] copies/mL. Following successful genotyping, the prevalence of high-risk oncogenic HPV was 36.32% (73/201), with a significantly higher proportion among those with HIV-infection (41.98% [55/131] vs. 25.71% [18/70]; p = 0.02; OR = 2.1). CVS revealed 31.74% (97) normal cervix; 38.91% (100) inflammation; 16.34% (42) low-grade squamous intra-epithelial lesion; 6.34% (18) high-grade squamous intra-epithelial lesion. Overall rate of cervical lesions was 23.34% (60/257), with a non-significantly higher proportion in HIV-infected participants (25.00% [46/184] versus 19.17% [14/73]; p = 0.31). Of relevance, the presence of high-risk oncogenic HPV was significantly associated with cervical lesions (p < 0.0001; OR = 5.07), with a higher risk of cervical lesion among HIV-positive (p < 0.0001 and OR = 5.67) versus HIV-negative (p = 0.03 and OR = 3.83). Conclusion Though oncogenic HPV appears as an independent factor of the occurrence of cervical lesions, the risk of cervical lesion is substantially higher among HIV/HPV co-infection compared to HPV-infection alone. Thus, prevention of cervical cancer should be prioritised for women living with HIV-infection in HPV-endemic settings.