Nelly Mugo1, Linda O Eckert2, Lydia Odero3, Stephen Gakuo3, Kenneth Ngure4, Connie Celum5, Jared M Baeten5, Ruanne V Barnabas5, Anna Wald6. 1. Kenya Medical Research Institute, Center for Clinical Research, Kenya; Department of Global Health, University of Washington, Seattle, WA, USA; Partners in Health Research and Development, Kenya. Electronic address: rwamba@uw.edu. 2. Department of Global Health, University of Washington, Seattle, WA, USA; Department of Obstetrics and Gynaecology, University of Washington, WA, USA. 3. Partners in Health Research and Development, Kenya. 4. Department of Global Health, University of Washington, Seattle, WA, USA; Department of Community Health, Jomo Kenyatta University of Agriculture and Technology, Kenya. 5. Department of Global Health, University of Washington, Seattle, WA, USA; Departments of Medicine, University of Washington, Seattle, WA, USA; Department of Epidemiology, University of Washington, Seattle, WA, USA. 6. Departments of Medicine, University of Washington, Seattle, WA, USA; Department of Epidemiology, University of Washington, Seattle, WA, USA; Department of Laboratory Medicine, University of Washington, Seattle, WA, USA; Vaccine and Infectious Diseases Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
Abstract
OBJECTIVES: HIV infected children remain at increased risk of HPV associated malignancies as they initiate sexual activity. Though they mount a vigorous immune response to the quadrivalent human papillomavirus (QHPV-6, -11,-16, and -18; Gardasil®) vaccine, durability of the immune response is uncertain. We assessed antibody responses to HPV 6, -11, -16 and -18 for up to 48 months following administration of quadrivalent human papillomavirus vaccine in HIV-infected girls and boys ages 9-14 years in Kenya. DESIGN: Of 178 girls and boys who had previously received three doses of the quadrivalent HPV vaccine, 176 enrolled into extended follow up for 4 years. HPV antibodies to -6, -11, -16 and -18 were measured at 24, 36 and 48 months after the first vaccine dose using the total immunoglobulin G immunoassay (IgG LIA). We evaluated the magnitude and trend in HPV vaccine response and the effect of plasma HIV-1 RNA on HPV vaccine response from month 24 to month 48 of follow up. RESULTS: At re-enrollment, 24 months after initial vaccination, median age of participants was 14 years (range 11-17); 167 (95%) were receiving antiretroviral therapy and 110 (66%) had plasma HIV RNA < 40 copies/mL. The rate of HPV seropositivity at 48 months was 83% for HPV-6; 80% for HPV-11; 90% for HPV-16; and 77% for HPV-18. There was a plateau in mean log10 HPV-specific antibody titer between month 24 and 48. The mean log10 HPV-type specific antibody titer for children with undetectable HIV viral load (<40) at the time of vaccination consistently remained higher for the 48 months of follow up compared to children with detectable viral load. CONCLUSION: Children with HIV infection may retain long term antibody response following HPV immunization. Further work to define whether HIV-infected children are protected from HPV acquisition with low levels of HPV antibodies is needed.
OBJECTIVES:HIV infectedchildren remain at increased risk of HPV associated malignancies as they initiate sexual activity. Though they mount a vigorous immune response to the quadrivalent human papillomavirus (QHPV-6, -11,-16, and -18; Gardasil®) vaccine, durability of the immune response is uncertain. We assessed antibody responses to HPV 6, -11, -16 and -18 for up to 48 months following administration of quadrivalent human papillomavirus vaccine in HIV-infectedgirls and boys ages 9-14 years in Kenya. DESIGN: Of 178 girls and boys who had previously received three doses of the quadrivalent HPV vaccine, 176 enrolled into extended follow up for 4 years. HPV antibodies to -6, -11, -16 and -18 were measured at 24, 36 and 48 months after the first vaccine dose using the total immunoglobulin G immunoassay (IgG LIA). We evaluated the magnitude and trend in HPV vaccine response and the effect of plasma HIV-1 RNA on HPV vaccine response from month 24 to month 48 of follow up. RESULTS: At re-enrollment, 24 months after initial vaccination, median age of participants was 14 years (range 11-17); 167 (95%) were receiving antiretroviral therapy and 110 (66%) had plasma HIV RNA < 40 copies/mL. The rate of HPV seropositivity at 48 months was 83% for HPV-6; 80% for HPV-11; 90% for HPV-16; and 77% for HPV-18. There was a plateau in mean log10 HPV-specific antibody titer between month 24 and 48. The mean log10 HPV-type specific antibody titer for children with undetectable HIV viral load (<40) at the time of vaccination consistently remained higher for the 48 months of follow up compared to children with detectable viral load. CONCLUSION:Children with HIV infection may retain long term antibody response following HPV immunization. Further work to define whether HIV-infectedchildren are protected from HPV acquisition with low levels of HPV antibodies is needed.
Authors: Ana Gradissimo; Viswanathan Shankar; Fanua Wiek; Lauren St Peter; Yevgeniy Studentsov; Anne Nucci-Sack; Angela Diaz; Sarah Pickering; Nicolas F Schlecht; Robert D Burk Journal: Viruses Date: 2021-08-05 Impact factor: 5.048
Authors: Gui Liu; Nelly R Mugo; Cara Bayer; Darcy White Rao; Maricianah Onono; Nyaradzo M Mgodi; Zvavahera M Chirenje; Betty W Njoroge; Nicholas Tan; Elizabeth A Bukusi; Ruanne V Barnabas Journal: EClinicalMedicine Date: 2022-02-19
Authors: Lisa Staadegaard; Minttu M Rönn; Nirali Soni; Meghan E Bellerose; Paul Bloem; Marc Brisson; Mathieu Maheu-Giroux; Ruanne V Barnabas; Melanie Drolet; Philippe Mayaud; Shona Dalal; Marie-Claude Boily Journal: EClinicalMedicine Date: 2022-08-03