Primary Keratinocytes Can Be Infected by Natural Isolates of Genital Human Papillomavirus

Intervirology ◽  
1995 ◽  
Vol 38 (5) ◽  
pp. 264-268 ◽  
Author(s):  
Aldo Venuti ◽  
Anna Di Lonardo ◽  
Lucio Standoli ◽  
Maria Luisa Marcante
Keyword(s):  
Human Papillomavirus ◽  
Primary Keratinocytes ◽  
Natural Isolates

scholarly journals Genome-wide analysis of high risk human papillomavirus E2 proteins in human primary keratinocytes

Genomics Data ◽  
2014 ◽  
Vol 2 ◽  
pp. 147-149 ◽  
Author(s):  
Nuchsupha Sunthamala ◽  
Chai Ling Pang ◽  
Francoise Thierry ◽  
Sebastien Teissier ◽  
Chamsai Pientong ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
High Risk ◽  
Primary Keratinocytes ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Human Primary Keratinocytes

scholarly journals Genome-Wide Transcriptome Analysis of Human Papillomavirus 16-Infected Primary Keratinocytes Reveals Subtle Perturbations Mostly due to E7 Protein Expression

2019 ◽  
Vol 94 (3) ◽  
Author(s):  
Malgorzata Bienkowska-Haba ◽  
Wioleta Luszczek ◽  
Katarzyna Zwolinska ◽  
Rona S. Scott ◽  
Martin Sapp
Keyword(s):  
Human Papillomavirus ◽  
Life Cycle ◽  
Host Cell ◽  
Cell Lines ◽  
Hpv Infection ◽  
Infection Model ◽  
Primary Keratinocytes ◽  
Pocket Proteins ◽  
Transcriptional Alterations ◽  
Transcriptional Changes

ABSTRACT It is established that the host cell transcriptomes of natural lesions, organotypic rafts, and human papillomavirus (HPV)-immortalized keratinocytes are altered in the presence of HPV genomes. However, the establishment of HPV-harboring cell lines requires selection and immortalization, which makes it impossible to distinguish between alterations directly induced by HPV or indirectly by the need for immortalization or selection. To address direct effects of HPV infection on the host cell transcriptome, we have used our recently established infection model that allows efficient infection of primary keratinocytes with HPV16 virions. We observed only a small set of genes to be deregulated at the transcriptional level at 7 days postinfection (dpi), most of which fall into the category regulated by pocket proteins pRb, p107, and p130. Furthermore, cell cycle genes were not deregulated in cells infected with a virus lacking E7 despite the presence of episomal genome and viral transcripts. These findings imply that the majority of transcriptional changes are due to the E7 protein impairing pocket protein function. Additional pathways, such as the Fanconi anemia-BRCA pathway, became perturbed only after long-term culturing of infected cells. When grown as organotypic raft cultures, keratinocytes infected with wild-type but not E7 mutant virus had perturbed transcriptional regulation of pathways previously identified in natural lesions and in rafts derived from immortalized keratinocytes. We conclude that the HPV infection model provides a valuable tool to distinguish immediate transcriptional alterations from those induced by persistent infection and the need for selection and immortalization. IMPORTANCE To establish infection and complete the viral life cycle, human papillomavirus (HPV) needs to alter the transcriptional program of host cells. Until recently, studies were restricted to keratinocyte-derived cell lines immortalized by HPV due to the lack of experimental systems to efficiently infect primary keratinocytes. Need for selection and immortalization made it impossible to distinguish between alterations induced by HPV and secondary adaptation due to selection and immortalization. With our recent establishment of an extracellular matrix (ECM)-to-cell transfer system allowing efficient infection of primary keratinocytes, we were able to identify transcriptional changes attributable to HPV16 infection. Most perturbed genes fall into the class of S-phase genes, which are regulated by pocket proteins. Indeed, infection with viruses lacking E7 abrogated most transcriptional changes. It is important to note that many transcriptional alterations thought to be important for the HPV life cycle are actually late events that may reflect immortalization and, possibly, disease progression.

scholarly journals UV-B irradiation stimulates the promoter activity of the high-risk, cutaneous human papillomavirus 5 and 8 in primary keratinocytes

2004 ◽  
Vol 150 (1) ◽  
pp. 145-151 ◽  
Author(s):  
B. Akg�l ◽  
W. Lemme ◽  
R. Garc�a-Escudero ◽  
A. Storey ◽  
H. J. Pfister
Keyword(s):  
Human Papillomavirus ◽  
High Risk ◽  
Promoter Activity ◽  
Primary Keratinocytes

Human papillomavirus type 5 in primary keratinocytes from psoriatic skin

2005 ◽  
Vol 14 (11) ◽  
pp. 824-829 ◽  
Author(s):  
Paola Simeone ◽  
Massimo Teson ◽  
Alessandra Latini ◽  
Massimo Carducci ◽  
Aldo Venuti
Keyword(s):  
Human Papillomavirus ◽  
Psoriatic Skin ◽  
Primary Keratinocytes

scholarly journals Inhibition of Human Papillomavirus Type 16 E7 Phosphorylation by the S100 MRP-8/14 Protein Complex

2005 ◽  
Vol 79 (2) ◽  
pp. 1099-1112 ◽  
Author(s):  
Sharof Tugizov ◽  
Jennifer Berline ◽  
Rossana Herrera ◽  
Maria Elena Penaranda ◽  
Mayumi Nakagawa ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Epithelial Cells ◽  
Protein Complex ◽  
Calcium Binding ◽  
Inhibitory Effect ◽  
Related Factor ◽  
Primary Keratinocytes ◽  
Viral Oncoprotein ◽  
Human Papillomavirus Type 16 ◽  
Oncogenic Activity

ABSTRACT The human papillomavirus type 16 (HPV16) E7 is a major viral oncoprotein that is phosphorylated by casein kinase II (CKII). Two S100 family calcium-binding proteins, macrophage inhibitory-related factor protein 8 (MRP-8) and MRP-14, form a protein complex, MRP-8/14, that inactivates CKII. The MRP-8/14 protein complex may inhibit CKII-mediated E7 phosphorylation and therefore may alter its interaction with cellular ligands and reduce E7 oncogenic activity. We examined the inhibitory effect of the MRP-8/14 complex on CKII activity and HPV16 E7 phosphorylation. We have shown that CKII activity and HPV16 E7 phosphorylation were inhibited by uptake of exogenous MRP-8/14 and activation of endogenous MRP-8/14. MRP-8/14-mediated inhibition of E7 phosphorylation occurred at the G1 phase of the cell cycle. Analysis of MRP expression in primary keratinocytes and in HPV16- and 18-transformed cervical and foreskin epithelial cell lines showed that expression of MRP-8, MRP-14, and the MRP-8/14 complex was detected only in primary untransformed keratinocytes and not in the HPV-infected immortalized epithelial cells. CKII activity in HPV-immortalized keratinocytes was approximately fourfold higher than in HPV-negative primary keratinocytes. Treatment of HPV-positive immortalized epithelial cells with exogenous MRP-8/14 resulted in E7 hypophosphorylation and complete inhibition of cell growth within 2 weeks, compared with HPV-negative primary and immortalized HPV-negative cervical epithelial cells, which showed 25 and 40% growth inhibition, respectively. Together these results suggests that the MRP-8/14 protein complex in HPV-infected epithelial cells may play an important role in regulation of CKII-mediated E7 phosphorylation and inhibition of its oncogenic activity.

A combined ultrastructural and gene molecular research for the relationship between human uterine cervical carcinoma and human papillomavirus

1990 ◽  
Vol 48 (3) ◽  
pp. 204-205
Author(s):  
Kun Lee ◽  
Jingyi Si ◽  
Ricai Han ◽  
Wei Zhang ◽  
Bingbing Tan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Intraepithelial Neoplasia ◽  
Hpv Infection ◽  
Dot Blot ◽  
Homologous Sequences ◽  
Normal Cervical Epithelium ◽  
The Relationship ◽  
Chronic Cervicitis

There are more supports for the view that human papillomavirus (HPV) infection might be an etiological factor in the development of cervical cancer when the association of persistent condylomata is considered. Biopsies from 318 cases with squamous cell carcinoma of uterine cervix, 48 with cervical and vulvar condylomata, 14 with cervical intraepithelial neoplasia (CIN), 34 with chronic cervicitis and 24 normal cervical epithelium were collected from 5 geographic regions of China with different cervical cancer mortalities. All specimens were prepared for Dot blot, Southern blot and in situ DNA-DNA hybridizations by using HPV-11, 16, 18 DNA labelled with 32P and 3H as probes to detect viral homologous sequences in samples. Among them, 32 cases with cervical cancer, 27 with condyloma and 10 normal cervical epitheliums were randomly chosen for comparative EM observation. The results showed that: 1), 192 out of 318 (60.4%) cases of cervical cancer were positive for HPV-16 DNA probe (Table I)

Epidemiology of Human Papillomavirus Infection

2000 ◽  
Vol 34 (6) ◽  
pp. 194-200 ◽  
Author(s):  
Joakim Dillner ◽  
Chris J. L. M. Meijer ◽  
Geo von Krogh ◽  
Simon Horenblas
Keyword(s):  
Human Papillomavirus ◽  
Human Papillomavirus Infection ◽  
Papillomavirus Infection
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