HLA-G and vertical mother-to-child transmission of human papillomavirus infection

Louvanto, Karolina; Roger, Michel; Faucher, Marie-Claude; Syrjänen, Kari; Grénman, Seija; Syrjänen, Stina

doi:10.1016/j.humimm.2018.03.002

Cited by 22 publications

(33 citation statements)

References 33 publications

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“…Among HPV-positive pregnant women in Brazil, a protective effect of the HLA-G * 01:01:02 allele against the occurrence of CIN was observed in a cohort of HPV/HIV co-infected pregnant women (101). In a study that focused on the role of host factors in the vertical transmission of HPV infection from mother to offspring, the results showed that the HLA-G * 01:01:01/01:04:01 genotype increased the risk of hrHPV infection in both cord blood and the infant's oral mucosa; moreover, the mother-child concordance of HLA-G * 01:01:02/01:01:02 increased the risk of oral hrHPV infection both in the mother and offspring (102). In addition, a pilot analysis of HLA-G promoter methylation and HPV infection status showed no association between HLA-G methylation and HPV infections in healthy women (103,104).…”

Section: Hla-g Polymorphisms In the Context Of Hpv Infectionsmentioning

confidence: 97%

“…Further evidence for the role of genetic factors in HPV infections and the carcinogenic process was provided by studies that showed an association with specific HLA-G coding region polymorphisms (96)(97)(98)(99)(100)(101)(102)(103)(104). Among the Canadian population, the HLA-G * 01:01:02 and HLA-G * 01:03 alleles were found to be related to an increased risk of HPV16 infection and persistent infections (96), while the HLA-G * 01:01:03 and HLA-G * 01:01:05 alleles were identified as significant predictors of cumulative coinfections over the follow-up period (97).…”

Section: Hla-g Polymorphisms In the Context Of Hpv Infectionsmentioning

confidence: 99%

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The Role of HLA-G in Human Papillomavirus Infections and Cervical Carcinogenesis

Xu¹,

Yan²,

Lin³

2020

Front. Immunol.

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Human leukocyte antigen (HLA)-G, a non-classical HLA-class I molecule, has a low polymorphism frequency, restricted tissue distribution and immunoinhibitory property. HLA-G expression in tumor cells and cells chronically infected with virus may enable them to escape from host immune surveillance. It is well-known that the HLA-G molecule is a novel biomarker and potential therapeutic target that is relevant in various types of cancers, but its role in cervical cancer has not been fully explored. In this review, we aim to summarize and discuss the immunologic role of the HLA-G molecule in the context of HPV infections and the process of cervical cancer carcinogenesis. A better understanding of the potential impact of HLA-G on the clinical course of persistent HPV infections, cervical epithelial cell transformation, tumor growth, recurrence and metastasis is needed to identify a novel diagnostic/prognostic biomarker for cervical cancer, which is critical for cervical cancer risk screening. In addition, it is also necessary to identify HLA-G-driven immune mechanisms involved in the interactions between host and virus to explore novel immunotherapy strategies that target HLA-G/immunoglobulin-like transcript (ILT) immune checkpoints.

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Section: Hla-g Polymorphisms In the Context Of Hpv Infectionsmentioning

confidence: 97%

Section: Hla-g Polymorphisms In the Context Of Hpv Infectionsmentioning

confidence: 99%

The Role of HLA-G in Human Papillomavirus Infections and Cervical Carcinogenesis

Xu¹,

Yan²,

Lin³

2020

Front. Immunol.

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“…The T-helper 2 cell cytokine profile might also predispose to persistent oral HPV-16 infection in women (34,125). We recently showed that the HLA-G allele concordance might affect the vertical transmission of HPV, especially to the oral cavity (126,127). We showed that the HLA-G genotype concordance of G * 01:01:01/ 01:04:01 increased the risk of positivity for the high-risk HPV genotype in umbilical cord blood and infant's oral mucosa.…”

Section: Hpv and Immunitymentioning

confidence: 99%

Oral manifestations of human papillomavirus infections

Syrjänen

2018

European J Oral Sciences

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123

144

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Papillomaviruses are one of the oldest viruses known, dating back 330 million years. During this long evolution, human papillomaviruses (HPV) have developed into hijackers of human cellular and immune systems in which they replicate and remain silent. Systematic studies on oral HPV infections and their outcomes are still scarce. Oral HPV infections have been linked to sexual behaviour, but recent evidence supports their horizontal, mouth‐to‐mouth, transmission. Most HPV infections in infants are acquired vertically from the mother during the intrauterine period, during delivery, or later via saliva. The best‐known benign clinical manifestations of HPV infection are oral papilloma/condyloma and focal epithelial hyperplasia. Evidence is emerging which suggests that some oral HPV infections might persist. Persistent HPV infection is mandatory for HPV‐associated malignant transformation. However, progression of HPV‐induced lesions to malignancy requires additional cofactors. In the early 1980s, we provided the first evidence that a subset of oral cancers and other head and neck cancers might be causally linked to HPV infection. This review summarizes current knowledge on the virus itself, its transmission modes, as well as the full spectrum of oral HPV infections – from asymptomatic infections to benign, potentially malignant oral lesions, and squamous cell carcinoma.

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“…Further, Lajoie et al explained that HLA-G re-expression has been suggested as a viral escape mechanism from immunosurveillance (15). Recently, Louvanto et al reported that HLA-G molecules played a role in the prediction of the likelihood of the newborn's for oral HPV infection at birth (16).…”

Section: Introductionmentioning

confidence: 99%

“…There are a few studies on the association between HLA-G polymorphisms with HPV infections (14–16). However, the interaction between HPV infection and HLA-G isoforms in tumors is relatively less explored.…”

Section: Introductionmentioning

confidence: 99%

Immune Modulation in HLA-G Expressing Head and Neck Squamous Cell Carcinoma in Relation to Human Papilloma Virus Positivity: A Study From Northeast India

Sarmah

Baruah

2019

Front. Oncol.

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Background: Tumor specific ectopic expression of the immunomodulatory molecule, HLA-G is known to mediate immune tolerance and promote carcinogenesis. Viruses too employ strategies to evade immune surveillance. Considering the role of both HLA-G and HPV in tumor growth and progression, it is pertinent to investigate the relationship between HLA-G and HPV in context of immune modulation in HNSCC. Method: A hospital based case–control study was conducted in histopathologically confirmed HNSCC tissues. HLA-G isoform expression and HPV association studies were carried out and mRNA levels of HLA-G, markers of proliferation and differentiation (ki-67, keratin 18, cyclin D1), immune checkpoint molecules (IL-10, PD-1. TGF-β), SOCS (SOCS1 and SOCS3) and pro-inflammatory cytokine IFN-γ were determined. Results: Higher expression of HLA-G was noted in HPV positive tumors (5.14 fold, p = 0.002). HLA-G7 was the most frequent isoform (29/80) found in HNSCC particularly in HPV positive tumors (13/16). In HPV negative tumors, all the checkpoint molecules were upregulated along with pro–inflammatory IFN-γ. In contrast, in HPV positive tumors, IFN-γ expression was higher (2.12 fold) but levels of IL-10, PD-1, TGF-β, SOCS1 and SOCS3 were markedly lower (fold change of IL-10 = 0.37, PD1 = 0.41, TGF-β = 0.17, SOCS1 = 0.055, SOCS3 = 0.027). HPV positive tumors were more proliferative and differentiated with higher expression of ki-67 and keratin18 (6.25 fold, p = 0.079 and 10.62 fold, p = 0.009). Decreased expression of cyclin D1 was noted in HPV positive tumors (6.94 fold, p = 0.006) than HPV negative tumors (17.69 fold). Also, HLA-G7 expressing HPV positive tumors showed lowest expression of cyclin D1. Interestingly, SOCS showed normal expression in HLA-G7 expressing HPV negative tumors (1.2 and 1.4 fold). IFN-γ was downregulated in HPV positive tumors without HLA-G7 (0.31 fold). Conclusion: Our data suggests that SOCS were downregulated irrespective of HLA-G positivity and IFN- γ expression appeared to be mediated by HLA-G. SOCS are reported to have anti-tumor activity and also SOCS and soluble HLA-G are known to interfere with cell cycle progression. Hence, through regulating HLA-G expression, HPV positive tumors could mediate immune suppression by manipulating SOCS, IFN-γ, IL-10 and cyclin D1 pathways which needs further exploration.

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HLA-G and vertical mother-to-child transmission of human papillomavirus infection

Cited by 22 publications

References 33 publications

The Role of HLA-G in Human Papillomavirus Infections and Cervical Carcinogenesis

The Role of HLA-G in Human Papillomavirus Infections and Cervical Carcinogenesis

Oral manifestations of human papillomavirus infections

Immune Modulation in HLA-G Expressing Head and Neck Squamous Cell Carcinoma in Relation to Human Papilloma Virus Positivity: A Study From Northeast India

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