Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Isaguliants, Maria; Bayurova, Ekaterina; Avdoshina, Darya; Kondrashova, A. S.; Chiodi, Francesca; Palefsky, Joel M.

doi:10.3390/cancers13020305

Cited by 50 publications

(50 citation statements)

References 193 publications

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“…In light of the emerging role of the microenvironment in promoting and sustaining the growth and survival of tumor cells ( 37 , 38 ), the possibility that HIV-1–encoded proteins derived from infected cells and endowed with peculiar biologic properties contribute to lymphomagenesis was entertained. A previous study has shown that a vp17 increases cell proliferation of Epstein–Barr virus–infected primary human B cells ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Binding to PI(4,5)P2 is indispensable for secretion of B-cell clonogenic HIV-1 matrix protein p17 variants

Bugatti

Caccuri

Filippini

et al. 2021

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Binding to PI(4,5)P2 is indispensable for secretion of B-cell clonogenic HIV-1 matrix protein p17 variants

Bugatti

Caccuri

Filippini

et al. 2021

Journal of Biological Chemistry

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“…Numerous studies have delineated the effect of HIV-1 infection on infection with HPVs/HR HPVs, development of HR HPV-associated lesions and eventually HPV-associated cancer. On the overall, HIV-1 infection modifies HPV pathogenesis and promotes cancer through multiple mechanisms related to complex HIV-induced immune suppression, dysfunction, and persistent inflammation [ 15 , 38 , 39 , 40 , 41 ], as well as direct oncogenic effects of HIV proteins, also in the cervix [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Prevalence and Risk Factors of Infection with High Risk Human Papilloma Viruses among HIV-Positive Women with Clinical Manifestations of Tuberculosis in a Middle-Income Country

et al. 2021

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Women living with HIV-1 are at high risk of infection with human papillomavirus of high carcinogenic risk (HR HPVs). M. tuberculosis (TB) promotes HPV infection and increases the risk to develop HPV-associated cancer. Our knowledge of persisting HR HPVs genotypes, and of the factors promoting HR HPV infection in people living with HIV-1 with clinical TB manifestations is sparse. Here, we analyzed 58 women living with HIV-1 with clinical TB manifestations (WLWH with TB) followed up in specialized centers in Russia, a middle income country endemic for HIV-1 and TB, for the presence in cervical smears of DNA of twelve HR HPV genotypes. DNA encoding HPV16 E5, E6/E7 was sequenced. Sociodemographic data of patients was collected by questionnaire. All women were at C2-C3 stages of HIV-infection (by CDC). The majority were over 30 years old, had secondary education, were unemployed, had sexual partners, experienced 2–3 pregnancies and at least one abortion, and were smokers. The most prevalent was HPV16 detected in the cervical smears of 38% of study participants. Altogether 34.5% of study participants were positive for HR HPV types other than HPV16; however, but none of these types was seen in more than 7% of tested samples. Altogether, 20.7% of study participants were positive for several HR HPV types. Infections with HPVs other than HPV16 were common among WLWH with generalized TB receiving combined ART/TB-therapy, and associated with their ability to work, indirectly reflecting both their health and lifestyle. The overall prevalence of HR HPVs was associated with sexual activity of women reflected by the number of pregnancies, and of HPV 16, with young age; none was associated to CD4+-counts, route of HIV-infection, duration of life with HIV, forms of TB-infection, or duration of ART, characterizing the immune status. Thus, WLWH with TB—especially young—were predisposed to infection with HPV16, advancing it as a basis for a therapeutic HPV vaccine. Phylogenetic analysis of HPV16 E5, E6/E7 DNA revealed no common ancestry; sequences were similar to those of the European and American HPV16 strains, indicating that HPV vaccine for WLWH could be the same as HPV16 vaccines developed for the general population. Sociodemographic and health correlates of HR HPV prevalence in WLWH deserve further analysis to develop criteria/recommendations for prophylactic catch-up and therapeutic HPV vaccination of this highly susceptible and vulnerable population group.

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“…While traditionally this enhanced risk was associated with HIV-1-induced immune suppression and exhaustion, as well as chronic B-cell activation, the advent of antiretroviral therapy (ART), even at early stages of infection, did not abolish this risk [ 51 ]. There is now enough experimental evidence to support an oncogenic role for HIV-1 and its antigens in carcinogenesis [ 52 ]. HIV-1 does not infect B lymphocytes; however, the virus is capable of binding these cells through cell surface receptors [ 20 ], and so can components of the virus, as has been demonstrated by binding of the p17 matrix protein to the CXCR receptors [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Modulation of Cellular MicroRNA by HIV-1 in Burkitt Lymphoma Cells—A Pathway to Promoting Oncogenesis

Ramorola

Goolam-Hoosen

Rios

et al. 2021

Genes

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Viruses and viral components have been shown to manipulate the expression of host microRNAs (miRNAs) to their advantage, and in some cases to play essential roles in cancer pathogenesis. Burkitt lymphoma (BL), a highly aggressive B-cell derived cancer, is significantly over-represented among people infected with HIV. This study adds to accumulating evidence demonstrating that the virus plays a direct role in promoting oncogenesis. A custom miRNA PCR was used to identify 32 miRNAs that were differently expressed in Burkitt lymphoma cells exposed to HIV-1, with a majority of these being associated with oncogenic processes. Of those, hsa-miR-200c-3p, a miRNA that plays a crucial role in cancer cell migration, was found to be significantly downregulated in both the array and in single-tube validation assays. Using an in vitro transwell system we found that this downregulation correlated with significantly enhanced migration of BL cells exposed to HIV-1. Furthermore, the expression of the ZEB1 and ZEB2 transcription factors, which are promotors of tumour invasion and metastasis, and which are direct targets of hsa-miR-200c-3p, were found to be enhanced in these cells. This study therefore identifies novel miRNAs as role players in the development of HIV-associated BL, with one of these miRNAs, hsa-miR-200c-3p, being a candidate for further clinical studies as a potential biomarker for prognosis in patients with Burkitt lymphoma, who are HIV positive.

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Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Cited by 50 publications

References 193 publications

Binding to PI(4,5)P2 is indispensable for secretion of B-cell clonogenic HIV-1 matrix protein p17 variants

Binding to PI(4,5)P2 is indispensable for secretion of B-cell clonogenic HIV-1 matrix protein p17 variants

Prevalence and Risk Factors of Infection with High Risk Human Papilloma Viruses among HIV-Positive Women with Clinical Manifestations of Tuberculosis in a Middle-Income Country

Modulation of Cellular MicroRNA by HIV-1 in Burkitt Lymphoma Cells—A Pathway to Promoting Oncogenesis

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