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Dendrimers as a Candidate for Microbicide in Prevention of HIV-1 Infection in Women: Steps toward Their Clinical Evaluation
Published in Costas Demetzos, Stergios Pispas, Natassa Pippa, Drug Delivery Nanosystems, 2019
Daniel Sepúlveda-Crespo, Jose Luis Jiménez-Fuentes, María Angeles Muñoz-Fernández
According to the Joint United Nations Programme on HIV and AIDS (UNAIDS) estimates, in 2015 more than 36.7 million people were living with HIV-1 globally, and women account for nearly 50% of the infected people (of these, 80% live in sub-Saharan Africa), who acquire HIV-1 mostly by heterosexual contact [64]. In the last 15 years reductions in new HIV infections and acquired immunodeficiency syndrome (AIDS)-related deaths have been generated. However, in order to reach the vision of zero new HIV infections, zero discrimination, and zero AIDS-related deaths, new targets need to be set [65]. The most common way to be infected with HIV-1 is through sexual exposure [66]. Women are more susceptible to HIV-1 than men due to hormonal changes, vaginal microbial ecology, and physiology, and a higher prevalence of STIs. The female genital tract is divided into three major parts: the vaginal mucosa, the ectocervix, and the endocervix [67]. The vaginal mucosa and the ectocervix are composed of a multilayered nonkeratinized stratified squamous epithelium, while the endocervix consists of a single-layered columnar epithelium. The intact vaginal epithelial cells have a limited permeability to particles larger than 30 nm. Cell-free HIV-1 enters vaginal epithelium by diffusing across a concentration gradient (transcytosis) and is recruited on the surface of epithelial cells until HIV-1 can be uptaken by intraepithelial Langerhans cells [68]. Successful transfer of HIV-1 results in HIV-1 uptake by dendritic cells (DCs) at the subepithelium and subsequent dissemination to draining lymph nodes. HIV-1-infected cells can also cross the epithelial barrier by physical abrasion or by transmigration [69, 70].
Optimal control in a multi-pathways HIV-1 infection model: a comparison between mono-drug and multi-drug therapies
Published in International Journal of Control, 2021
Chittaranjan Mondal, Debadatta Adak, Nandadulal Bairagi
Human immunodeficiency virus type-1 (HIV-1) is a deadly pathogen that infects cells, one type of immune cells. The gradual depletion of cells in blood plasma is the signature of HIV-1 infection. AIDS (Acquired Immunodeficiency Syndrome) develops when the cells count drops to 200 cells/ from its normal value of 1000 cells/ (Wodarz & Levy, 2007). In reduced level of cells, the immune system cannot act properly. As a result, an HIV infected individual becomes susceptible to different opportunistic infections.
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Human immunodeficiency virus-1 (HIV-1) is the causative agent of acquired immune deficiency syndrome (AIDS). HIV-1 is a RNA virus that transcribes its RNA core into DNA through the action of reverse transcriptase, which subsequently is integrated in the host cell DNA. This virus primarily infects CD4-positive T-cells, macrophages and dendritic cells. There is no evidence that HIV-1 causes cancer directly. However HIV-1 increases cancer risk because it gives rise to a severe immunodeficiency, leading to an enhanced risk from secondary carcinogens. For example, the risk of non-Hodgkin’s lymphoma is enhanced as a result of ‘the profound depletion of CD4-positive T lymphocytes that is caused by HIV-1 and allows the dysregulation of B-cell control, and the expression of the effects of lymphotrophic viruses’ (IARC 2012b, 223). Despite the integration of the cDNA transcript of the viral RNA in the genome, there is no apparent evidence that HIV induces chromosomal or genetic damage.