The interaction between human papillomavirus and other viruses

Guidry, Jessie; Scott, Rona S.

doi:10.1016/j.virusres.2016.11.002

Cited by 104 publications

(141 citation statements)

References 143 publications

Supporting

Mentioning

133

Contrasting

Unclassified

Order By: Relevance

“…Additional evidence of a biological dose–response also comes from studies comparing HPV acquisition and clearance by CD4 levels among PLHIV only, which was not the purpose of our study . The associations found are also biologically plausible . HIV may increase susceptibility to HPV infection and persistence of HPV infection among PLHIV due to immunodeficiency, the inflammatory response to HIV infection, immune dysregulation at the site of HIV infection, and/or the effects of HIV on HPV transcription and translation .…”

Section: Resultsmentioning

confidence: 74%

Evidence of synergistic relationships between HIV and Human Papillomavirus (HPV): systematic reviews and meta‐analyses of longitudinal studies of HPV acquisition and clearance by HIV status, and of HIV acquisition by HPV status

et al. 2018

View full text Add to dashboard Cite

IntroductionObservational studies suggest HIV and human papillomavirus (HPV) infections may have multiple interactions. We reviewed the strength of the evidence for the influence of HIV on HPV acquisition and clearance, and the influence of HPV on HIV acquisition.MethodsWe performed meta‐analytic systematic reviews of longitudinal studies of HPV incidence and clearance rate by HIV status (review 1) and of HIV incidence by HPV status (review 2). We pooled relative risk (RR) estimates across studies using random‐effect models. I 2 statistics and subgroup analyses were used to quantify heterogeneity across estimates and explore the influence of participant and study characteristics including study quality. Publication bias was examined quantitatively with funnel plots and subgroup analysis, as well as qualitatively.Results and DiscussionIn review 1, 37 publications (25 independent studies) were included in the meta‐analysis. HPV incidence (pooled RR = 1.55, 95% CI: 1.29 to 1.88; heterosexual males: pooled RR = 1.95, 95% CI: 1.62, 2.34; females: pooled RR = 1.63, 95% CI: 1.26 to 2.11; men who have sex with men: pooled RR = 1.36, 95% CI: 1.01 to 1.82) and high‐risk HPV incidence (pooled RR = 2.20, 95% CI: 1.90 to 2.54) was approximately doubled among people living with HIV (PLHIV) whereas HPV clearance rate (pooled RR = 0.53, 95% CI: 0.42 to 0.67) was approximately halved. In review 2, 14 publications (11 independent studies) were included in the meta‐analysis. HIV incidence was almost doubled (pooled RR = 1.91, 95% CI 1.38 to 2.65) in the presence of prevalent HPV infection. There was more evidence of publication bias in review 2, and somewhat greater risk of confounding in studies included in review 1. There was some evidence that adjustment for key confounders strengthened the associations for review 2. Misclassification bias by HIV/HPV exposure status could also have biased estimates toward the null.ConclusionsThese results provide evidence for synergistic HIV and HPV interactions of clinical and public health relevance. HPV vaccination may directly benefit PLHIV, and help control both HPV and HIV at the population level in high prevalence settings. Our estimates of association are useful for mathematical modelling. Although observational studies can never perfectly control for residual confounding, the evidence presented here lends further support for the presence of biological interactions between HIV and HPV that have a strong plausibility.

show abstract

Section: Resultsmentioning

confidence: 74%

Evidence of synergistic relationships between HIV and Human Papillomavirus (HPV): systematic reviews and meta‐analyses of longitudinal studies of HPV acquisition and clearance by HIV status, and of HIV acquisition by HPV status

et al. 2018

View full text Add to dashboard Cite

show abstract

“…However, the direct mechanism is not clear (45)(46)(47). Additionally, the effects of duration of HAART use in cervical carcinogenesis prevention are still unknown (48,49).…”

Section: I) Cervical Cancer Pathogenesis Haart and Hiv/hpv Co-infectionmentioning

confidence: 99%

“…HIV proteins can directly cause cancer growth by interfering with cellular functions (8,42,49,53). For example, HIV Tat proteins directly interact with the host tumour suppressor genes p53/pRb/p130/p107 and induce increased cell proliferation, which promote the effect of HPV oncoproteins E6 and E7 in the rapidly progressing cervical carcinogenesis (33,42,49,53,54). The increased rate of HPV-associated cervical disease in HIV positive women is aggravated by HIV/HPV molecular interactions because HIV Tat proteins can modulate HPV E2 gene expression, which in turn, influences HPV viral replication (55,56).…”

Section: I) Cervical Cancer Pathogenesis Haart and Hiv/hpv Co-infectionmentioning

confidence: 99%

Impact of Host Molecular Genetic Variations and HIV/HPV Co-infection on Cervical Cancer Progression: A Systematic review

Chambuso¹,

Gray²,

Kaambo³

et al. 2018

Oncomedicine

View full text Add to dashboard Cite

Only a small subset of women who are co-infected with Human Immunodeficiency Virus sub-type 1 (HIV) and persistence oncogenic Human papillomavirus (HPV), progress rapidly to invasive cervical cancer by mechanisms that are currently poorly understood. The use of Highly Active Antiretroviral Therapy (HAART), with ensuing immune reconstitution of CD4 T-cells, does not appear to prevent rapidly progressing cervical carcinogenesis. Therefore, to better understand the cervical cancer pathogenesis in HIV/HPV co-infected women, this review focuses on identifying host molecular genetic variations and genetic alterations in cervical cancer progression that may play a role in disease progression. This is an important aspect for individualised genomic profiling and targeted molecular prevention in order to improve the management of the disease in this sub-population.

show abstract

“…For example, viruses such as the Epstein Barr virus (EBV), the Kaposi’s sarcoma herpesvirus (KSHV), human immunodeficiency virus type 1 (HIV-1), human hepatitis C virus (HCV) show association with non-Hodgkin’s lymphomas (13). Co-infection of any one or multiple viruses may establish an environment that enhances tumor initiation and progression (14, 15). In additional to clinical phenotype, experimental models of co-infection have identified a variety of mechanisms that might contribute to tumorigenesis, including viral cofactors (16-18), common signalling pathway targets (18, 19), epigenetic modifications (reprogramming) (20-23), microenvironmental abnormalities (13) and interference with cell death (24, 25).…”

Section: Introductionmentioning

confidence: 99%

ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147

Zhou

Xue

Zhuang

et al. 2018

Preprint

View full text Add to dashboard Cite

22The tumorigenesis is the result of the accumulation of multiple oncogenes and tumor 23 suppressor genes changes. Co-infection of avian leucosis virus subgroup J (ALV-J) 24 and reticuloendotheliosis virus ( REV) , as two oncogenic retroviruses, showed 25 synergistic pathogenic effects characterized by enhanced tumor initiation and 26 progression. The molecular mechanism underlying synergistic effects of ALV-J and 27 REV on the neoplasia remains unclear. Here, we found co-infection of ALV-J and 28 REV enhanced the ability of virus infection, increased viral life cycle, maintained cell 29 survival and enhanced tumor formation. We combined the high-throughput proteomic 30 readout with a large-scale miRNA screening to identify which molecules are involved 31 in the synergism. Our results revealed co-infection of ALV-J and REV activated a 32 latent oncogene of KIAA1199 and inhibited the expression of tumor suppressor miR-33 147. Further, enhanced KIAA1199, down-regulated miR-147, activated NF-κB and 34 EGFR were demonstrated in co-infected tissues and tumor. Mechanistically, we 35 showed ALV-J and REV synergistically enhanced KIAA1199 by activation of NF-κB 36 and EGFR signalling pathway, and the suppression of tumor suppressor miR-147 37 was contributed to maintain the NF-κB/KIAA1199/EGFR pathway crosstalk by 38 targeting the 3'UTR region sequences of NF-κB p50 and KIAA1199. Our results 39 contributed to the understanding of the molecular mechanisms of viral synergistic 40 tumorgenesis, which provided the evidence that suggested the synergistic actions of 41 two retroviruses could result in activation of latent pro-oncogenes. 42 Author summary 3 43The tumorigenesis is the result of the accumulation of multiple oncogenes and tumor 44 suppressor genes changes. Co-infection with ALV-J and REV showed synergistic 45 pathogenic effects characterized by enhanced tumor progression, however, the 46 molecular mechanism on the neoplasia remains unclear. Our results revealed co-47 infection of ALV-J and REV promotes tumorigenesis by both induction of a latent 48 oncogene of KIAA1199 and suppression of the expression of tumor suppressor miR-49 147. Mechanistic studies revealed that ALV-J and REV synergistically enhance 50 KIAA1199 by activation of NF-κB and EGFR signalling pathway, and the suppression 51 of tumor suppressor miR-147 was contributed to maintain the NF-52 κB/KIAA1199/EGFR pathway crosstalk by targeting the 3'UTR region sequences of 53 NF-κB p50 and KIAA1199. These results provided the evidence that suggested the 54 synergistic actions of two retroviruses could result in activation of latent pro-55 oncogenes, indicating the potential preventive target and predictive factor for ALV-J 56 and REV induced tumorigenesis. 57 Introduction 58 Viral synergism occurs commonly in the nature when co-infection of two or more 59 unrelated viruses invades the same host. As two oncogenic retroviruses, avian 60 leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) are the 61 optimal model to study the synergisti...

show abstract

The interaction between human papillomavirus and other viruses

Cited by 104 publications

References 143 publications

Evidence of synergistic relationships between HIV and Human Papillomavirus (HPV): systematic reviews and meta‐analyses of longitudinal studies of HPV acquisition and clearance by HIV status, and of HIV acquisition by HPV status

Evidence of synergistic relationships between HIV and Human Papillomavirus (HPV): systematic reviews and meta‐analyses of longitudinal studies of HPV acquisition and clearance by HIV status, and of HIV acquisition by HPV status

Impact of Host Molecular Genetic Variations and HIV/HPV Co-infection on Cervical Cancer Progression: A Systematic review

ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147

Contact Info

Product

Resources

About