ArticleViruses2022
Dynamics of HIV-1/HTLV-I Co-Infection Model with Humoral Immunity and Cellular Infection.
Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
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Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus type 1 (HIV-1) and human T-lymphotropic virus type I (HTLV-I) are two retroviruses which infect the same target, CD4+ T cells. This type of cell is considered the main component of the immune system. Since both viruses have the same means of transmission between individuals, HIV-1-infected patients are more exposed to the chance of co-infection with HTLV-I, and vice versa, compared to the general population. The mathematical modeling and analysis of within-host HIV-1/HTLV-I co-infection dynamics can be considered a robust tool to support biological and medical research. In this study, we have formulated and analyzed an HIV-1/HTLV-I co-infection model with humoral immunity, taking into account both latent HIV-1-infected cells and HTLV-I-infected cells. The model considers two modes of HIV-1 dissemination, virus-to-cell (V-T-C) and cell-to-cell (C-T-C). We prove the nonnegativity and boundedness of the solutions of the model. We find all steady states of the model and establish their existence conditions. We utilize Lyapunov functions and LaSalle's invariance principle to investigate the global stability of all the steady states of the model. Numerical simulations were performed to illustrate the corresponding theoretical results. The effects of humoral immunity and C-T-C transmission on the HIV-1/HTLV-I co-infection dynamics are discussed. We have shown that humoral immunity does not play the role of clearing an HIV-1 infection but it can control HIV-1 infection. Furthermore, we note that the omission of C-T-C transmission from the HIV-1/HTLV-I co-infection model leads to an under-evaluation of the basic HIV-1 mono-infection reproductive ratio.
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