Human immunodeficiency virus (HIV) is an enveloped, positive sense single-stranded RNA virus that belongs to the Retroviridae family. HIV infects and destroys immune cells that express CD4 and CCR5. People living with HIV/AIDS are susceptible to developing cancer due to secondary immune dysfunction characterized by a gradual and steady decline in the activators and controllers of the immune system. This results in reduced immune reactivity against cancer cells. Human oncogenic viruses include Hepatitis B virus, Epstein-Barr virus, Human papillomavirus, Human T-cell leukemia virus 1, Hepatitis C virus, Human Herpesvirus type 8, and Merkel cell polyomavirus can cause chronic and/or latent infection in humans following primary infection. Individuals with HIV who are co-infected with oncogenic viruses are prone to developing cancer with waning cell-mediated immunity.Oncogenic viruses inactivate the checkpoint pathway to facilitate continued cellular proliferation and to prevent apoptosis of virally infected cells. Additionally, HIV transactivator protein (Tat) released from infected cells along with the overexpression of viral oncoproteins play a role in accelerated oncogenesis in people living with HIV in spite of compliance with antiretroviral therapy. Human cytomegalovirus is a ssDNA virus that causes chronic infection and latently infects hematopoietic stem cells. Furthermore, the oncomodulatory activity and oncogenic potential of human cytomegalovirus that facilitates the survival and metastasis of cancer particularly in individuals with HIV seropositivity is an area of active research.The purpose of this special issue is to highlight current research on the cellular and molecular mechanisms of cancer in people living with HIV. Thus, we welcome all researchers working on basic, translational, and clinical research in the field of oncogenic cancer in people living with HIV to submit original research, review articles, and short communications that will broaden our current understanding of these mechanisms that induce the malignant cellular transformations that culminate in the development of cancer.
Human immunodeficiency virus (HIV) is an enveloped, positive sense single-stranded RNA virus that belongs to the Retroviridae family. HIV infects and destroys immune cells that express CD4 and CCR5. People living with HIV/AIDS are susceptible to developing cancer due to secondary immune dysfunction characterized by a gradual and steady decline in the activators and controllers of the immune system. This results in reduced immune reactivity against cancer cells. Human oncogenic viruses include Hepatitis B virus, Epstein-Barr virus, Human papillomavirus, Human T-cell leukemia virus 1, Hepatitis C virus, Human Herpesvirus type 8, and Merkel cell polyomavirus can cause chronic and/or latent infection in humans following primary infection. Individuals with HIV who are co-infected with oncogenic viruses are prone to developing cancer with waning cell-mediated immunity.Oncogenic viruses inactivate the checkpoint pathway to facilitate continued cellular proliferation and to prevent apoptosis of virally infected cells. Additionally, HIV transactivator protein (Tat) released from infected cells along with the overexpression of viral oncoproteins play a role in accelerated oncogenesis in people living with HIV in spite of compliance with antiretroviral therapy. Human cytomegalovirus is a ssDNA virus that causes chronic infection and latently infects hematopoietic stem cells. Furthermore, the oncomodulatory activity and oncogenic potential of human cytomegalovirus that facilitates the survival and metastasis of cancer particularly in individuals with HIV seropositivity is an area of active research.The purpose of this special issue is to highlight current research on the cellular and molecular mechanisms of cancer in people living with HIV. Thus, we welcome all researchers working on basic, translational, and clinical research in the field of oncogenic cancer in people living with HIV to submit original research, review articles, and short communications that will broaden our current understanding of these mechanisms that induce the malignant cellular transformations that culminate in the development of cancer.