Determining the HPV vaccine schedule for a HIV-infected population in sub Saharan Africa, a commentary

Abstract

BackgroundEpidemiological studies have established human papillomavirus (HPV) infection as the central cause of invasive cervical cancer (ICC) and its precursor lesions. HIV is associated with a higher prevalence and persistence of a broader range of high-risk HPV genotypes, which in turn results in a higher risk of cervical disease. Recent WHO HPV vaccination schedule recommendations, along with the roll out of HAART at an earlier CD4 count within the female HIV-infected population, may have programmatic implications for sub Saharan Africa. This communication identifies research areas, which will need to be addressed for determining a HPV vaccine schedule for this population in sub Saharan Africa. A review of WHO latest recommendations and the evidence concerning one-dose HPV vaccine schedules was undertaken.ConclusionFor females ≥15 years at the time of first dose and immunocompromised and/or HIV-infected, a 3-dose schedule (0, 1–2, 6 months) is recommended for all three vaccines. There is some evidence that there is similar protection against HPV 16 and 18 infection from a single vaccination than from two or three doses, however there is no cross protection conferred to other genotypes. There is a need for periodic prevalence studies to determine the vaccination coverage of bivalent, quadrivalent and nonavalent vaccine targeted oncogenic HPV genotypes in women with CIN 3 or ICC at national level. In light of the increasing number of sub Saharan HIV-infected girls initiating HAART at a CD4 count above 350 mm3, there are a number of clinical, virological and public health research gaps to address before a tailored vaccine schedule can be established for this population.

Cervical Dysplasia, Infection, and Phylogeny of Human Papillomavirus in HIV-Infected and HIV-Uninfected Women at a Reproductive Health Clinic in Nairobi, Kenya

“…This high HPV 52 prevalence has also been observed in Zambia and China [ 42 , 43 ]. A high prevalence of HPV 53 in a HIV-infected woman with invasive cancer in a study done in Mombasa Kenya also confirms the potential role of other high-risk genotypes in cervical cancer genesis especially in HIV-infected women [ 13 , 14 ]. This is an indication that other HPV types are more prevalent in Kenya other than the two high-risk types included in the HPV vaccine.…”

“…Other studies seem to differ on this showing that Cervarix vaccine offers crossprotection to HPV 31, 33, and 45 [11]. A 9 valent vaccine with HPV 16,18,11,6,31,33,45,52, and 58 is estimated to prevent up to 90% of all cancers [12][13][14]. However, this vaccine is expensive and does not prevent infection beyond the 9 HPV types in the vaccine but is still a better alternative for sub-Saharan Africa [12].…”

“…Likewise, antibodies against HPV 16 will cross-react with HPV 33, 35, 52, and 58 from the same species (species 9) but not with HPV 18 and 45. However, Menon et al, suggest that this cross-reactivity is not achieved with a single-dose vaccination schedule [ 14 ]. Other studies seem to differ on this showing that Cervarix vaccine offers cross-protection to HPV 31, 33, and 45 [ 11 ].…”

“…There are three main vaccines for cervical cancer: a bivalent vaccine (Cervarix) that contains HPV 16 and 18 only, a quadrivalent vaccine (Gardasil) that has HPV 6,11,16,and 18, and a 9 valent vaccine with HPV 16,18,11,6,31,33,45,52, and 58 [11,12]. These vaccines are a breakthrough for cancer prevention since they have the HPV genotypes that are most oncogenic [13,14]. However, other high-risk types seem to be playing important roles in cervical cancer etiology.…”

Investigation of Cervical Tumor Biopsies for Chromosomal Loss of Heterozygosity (LOH) and Microsatellite Instability (MSI) at the HLA II Locus in HIV-1/HPV Co-infected Women

“…These precancerous lesions in HIV-1/HPV co-infected women are more aggressive, but only a small subset progress rapidly to invasive cervical cancer (ICC). This progression is unrelated to CD4 counts or antiretroviral (ARV) therapy (2, 3). What is not clear, however, is how and why this rapid cervical carcinogenesis is only observed in some HIV-1/HPV co-infected women (4).…”