α6 integrin is not the obligatory cell receptor for bovine papillomavirus type 4

Sibbet, Gary; Romero-Graillet, Christine; Meneguzzi, Guerríno; Campo, M. Saveria

doi:10.1099/0022-1317-81-2-327

Cited by 34 publications

(10 citation statements)

References 51 publications

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“…The micro-injury is necessary for the virus to access basal keratinocytes (Liu and Baleja, 2008), where the virus cycle begins (Campo, 1997a). Current studies also show that integrin α6 (CD49f) and integrin 332 (laminin 5) are targets for L1 binding (Sibbet et al , 2000; Florin et al , 2012). …”

Section: Bpv Infection Pathway and Histopathological Alterationsmentioning

confidence: 87%

Papillomaviruses: a systematic review

et al. 2017

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In the last decades, a group of viruses has received great attention due to its relationship with cancer development and its wide distribution throughout the vertebrates: the papillomaviruses. In this article, we aim to review some of the most relevant reports concerning the use of bovines as an experimental model for studies related to papillomaviruses. Moreover, the obtained data contributes to the development of strategies against the clinical consequences of bovine papillomaviruses (BPV) that have led to drastic hazards to the herds. To overcome the problem, the vaccines that we have been developing involve recombinant DNA technology, aiming at prophylactic and therapeutic procedures. It is important to point out that these strategies can be used as models for innovative procedures against HPV, as this virus is the main causal agent of cervical cancer, the second most fatal cancer in women.

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Section: Bpv Infection Pathway and Histopathological Alterationsmentioning

confidence: 87%

Papillomaviruses: a systematic review

et al. 2017

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“…It was speculated that this cleavage is required for cell surface localization of α6 integrin [50]. While data suggest that α6 integrin is required for HPV16 PsV infection, studies conducted with HPV33 and BPV4 concluded that α6 integrin is not required for infection [23, 51]. …”

Section: Binding and Cell Surface Receptors Of Hpv16mentioning

confidence: 99%

HPV entry into cells

Aksoy

Gottschalk

Meneses

2017

Mutation Research/Reviews in Mutation Research

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Human papillomavirus (HPV) is a sexually transmitted virus responsible for the development of cervical cancer, anal cancer, head and throat cancers, as well as genital area warts. A major focus of current HPV research is on preventing the virus from entering a cell and transferring its genetic material to the nucleus, thus potentially preventing the development of cancer. Although the available HPV vaccines are extremely successful, approximately 15 additional cancer-causing HPVs have been identified that the vaccines do not protect against. Therefore, roughly 150,000 cancer cases will not be prevented annually with the current vaccines. Research efforts focused on the basic cell biology of HPV infection have a goal of identifying common infectious events that may lead to inexpensive vaccines or anti-virals to prevent infection by most, if not all, HPVs. In this review we attempt to summarize what is known regarding the process of HPV binding, entry, and intracellular trafficking.

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“…One candidate that has been suggested based on in vitro studies is α6-integrin, an epithelial cell adhesion molecule [26]. However, some cell lines devoid of α6-integrin are readily infected, so it certainly is not an obligatory cell surface receptor for in vitro infection [27,28]. …”

Section: Entrymentioning

confidence: 99%

Current understanding of the mechanism of HPV infection

Schiller

Day

Kines

2010

Gynecologic Oncology

265

249

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HPVs (human papillomaviruses) and other papillomaviruses have a unique mechanism of infection that has likely evolved to limit infection to the basal cells of stratified epithelium, the only tissue in which they replicate. Recent studies in a mouse cervicovaginal challenge model indicate that, surprisingly, the virus cannot initially bind to keratinocytes in vivo. Rather it must first bind via its L1 major capsid protein to heparan sulfate proteoglycans (HSPGs) on segments of the basement membrane (BM) exposed after epithelial trauma and undergo a conformational change that exposes the N-terminus of L2 minor capsid protein to furin cleavage. L2 proteolysis exposes a previously occluded surface of L1 that binds an as yet undetermined cell surface receptor on keratinocytes that have migrated over the BM to close the wound. Papillomaviruses are the only viruses that are known to initiate their infectious process at an extracellular site. In contrast to the in vivo situation, the virions can bind directly to many cultured cell lines through cell surface HSPGs and then undergo a similar conformational change and L2 cleavage. Transfer to the secondary receptor leads to internalization, uncoating in late endosomes, escape from the endosome by an L2-dependent mechanism, and eventual trafficking of an L2–genome complex to specific subnuclear domains designated ND10 bodies, where viral gene transcription is initiated. The infectious process is remarkably slow and asynchronous both in vivo and in cultured cells, taking 12–24 h for initiation of transcription. The extended exposure of antibody neutralizing determinants while the virions reside on the BM and cell surfaces might, in part, account for the remarkable effectiveness of vaccines based on neutralizing antibodies to L1 virus-like particles or the domain of L2 exposed after furin cleavage.

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α6 integrin is not the obligatory cell receptor for bovine papillomavirus type 4

Cited by 34 publications

References 51 publications

Papillomaviruses: a systematic review

Papillomaviruses: a systematic review

HPV entry into cells

Current understanding of the mechanism of HPV infection

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