2022
DOI: 10.1128/spectrum.03622-22
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HIV-1 Proteins gp120 and Tat Promote Epithelial-Mesenchymal Transition and Invasiveness of HPV-Positive and HPV-Negative Neoplastic Genital and Oral Epithelial Cells

Abstract: HPV-16-immortalized genital and oral epithelial cells and HPV-negative oral cancer cells that undergo prolonged contact with cell-free HIV-1 virions or with viral proteins gp120 and tat respond by becoming more invasive. EMT cells induced by HIV-1 in cultures of HPV-16-immortalized anal and cervical epithelial cells express the stem cell markers CD133 and CD44.

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Cited by 12 publications
(11 citation statements)
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“…However, HIV 1 and its virulence proteins (gp120 and tat) exposure to the HPV 16 immortalised cell lines advanced the EMT transition and further metastasis. The same results were observed in the HPV‐negative cell line 98 . The correlation between OSCC and HIV‐HPV confection is not studied.…”
Section: Hiv and Hpv Virus Impact On Osccsupporting
confidence: 53%
See 1 more Smart Citation
“…However, HIV 1 and its virulence proteins (gp120 and tat) exposure to the HPV 16 immortalised cell lines advanced the EMT transition and further metastasis. The same results were observed in the HPV‐negative cell line 98 . The correlation between OSCC and HIV‐HPV confection is not studied.…”
Section: Hiv and Hpv Virus Impact On Osccsupporting
confidence: 53%
“…The same results were observed in the HPV-negative cell line. 98 The correlation between OSCC and HIV-HPV confection is not studied. The molecular mechanism must be explored to determine possible treatment options.…”
Section: Hiv and Hpv Virus Impact On Osccmentioning
confidence: 99%
“…Increased production of TGF-β which promotes immunosuppression was noted in HIV and also in simian immunodeficiency virus (SIV) infection. An enhanced intestinal TGF-β/Smad-dependent signaling in SIV-infected rhesus macaques was reported by Boby et al (2021) [ 233 ].…”
Section: Roles Of Tgf β In Viral Infection At the Non-maternal–fetal ...mentioning
confidence: 78%
“…Both gp120 and RT increase the expression of HPV16 E6 in HPV16 infected immortalized and/or completely transformed epithelial cells, while other HIV-1 proteins, such as capsid protein p24, had no effect [ 2 ]. Furthermore, the prolonged interaction of HIV-1 proteins gp120 and tat and cell-free HIV-1 virions with HPV16-immortalized anal, cervical, and oral epithelial cells was found to stimulate EMT and increase the invasiveness of HPV16-infected cells [ 47 , 48 ]. Overall, these data indicate that the presence of HIV-1 and/or its antigens in HPV16-infected neoplastic cells may potentiate HPV-associated tumorigenicity, making HIV-1 infection an integral part of the process of HPV-associated tumorigenesis.…”
Section: Introductionmentioning
confidence: 99%