Abstract
Human immunodeficiency virus (HIV)-infected patients are at an increased risk of co-infection with human papilloma virus (HPV), and subsequent malignancies such as oral cancer. To determine the role of HIV-associated immune suppression on HPV persistence and pathogenesis, and to investigate the mechanisms underlying the modulation of HPV infection and oral cancer by HIV, we developed a mathematical model of HIV/HPV co-infection. Our model captures known immunological and molecular features such as impaired HPV-specific effector T helper 1 (Th1) cell responses, and enhanced HPV infection due to HIV. We used the model to determine HPV prognosis in the presence of HIV infection, and identified conditions under which HIV infection alters HPV persistence in the oral mucosa system. The model predicts that conditions leading to HPV persistence during HIV/HPV co-infection are the permissive immune environment created by HIV and molecular interactions between the two viruses. The model also determines when HPV infection continues to persist in the short run in a co-infected patient undergoing antiretroviral therapy. Lastly, the model predicts that, under efficacious antiretroviral treatment, HPV infections will decrease in the long run due to the restoration of CD4+ T cell numbers and protective immune responses.
Highlights
Infection with the human immunodeficiency virus (HIV) afflicts over 35 million people worldwide and results in impaired immune responses which may affect defenses against other pathogens
The model presented here is a mechanistic ordinary differential equation (ODE)-based model that studies the dynamical interaction between the host and two virus populations: HIV and human papillomavirus (HPV)
To address the possible interactions leading to HPV persistence, we highlighted specific scenarios presenting an increased persistence of HPV due to the permissive immune environment created in an HIV-infected individual
Summary
Infection with the human immunodeficiency virus (HIV) afflicts over 35 million people worldwide and results in impaired immune responses which may affect defenses against other pathogens. Apart from the acquired immunodeficiency syndrome (AIDS), HIV increases the risk of developing opportunistic infections by other infectious agents, including viruses: papillomavirus, herpesviruses, flaviviruses; and bacteria: Helicobacter pylori, Salmonella typhimurium, Chlamydophila pneumonia [4]. Epidemiological data suggests that HIV patients have an increased risk for developing human papillomavirus (HPV)-induced cancers such as oropharyngeal cancer, cervical cancer, anogenital cancer and anal cancers [5,6,7,8,9,10]. The cellular and molecular mechanisms explaining the correlation between increased susceptibility of HPV-associated diseases and HIV-induced immune suppression remain largely unknown
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