Human papillomavirus type 11 alters the transcription and expression of loricrin, the major cell envelope protein

Elizabeth Lehr, Michael Jarnik, Darron Brown

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Human papillomavirus (HPV) does not induce lysis of infected keratinocytes, and the exact mechanisms of viral escape are not known. As keratinocytes differentiate, the cornified cell envelope (CCE) develops, providing a protective barrier to the host. We previously showed that the normally durable CCE in HPV 11-infected epithelium is fragile compared to CCEs in healthy epithelium. In this study, we examined uninfected and HPV 11-infected human genital epithelium for expression of loricrin, the major CCE protein in healthy epidermis. In HPV 11-infected human genital epithelium, detection of loricrin was reduced in immunoelectron microscopic and immunoblot assays, suggesting that loricrin incorporation into the CCE was reduced or that loricrin synthesis was reduced. Loricrin detection was reduced in immunohistochemical assays in areas of high viral replication. Mathematical modeling by least squares was performed using the amino acid composition of highly purified CCE fragments, confirming that loricrin was markedly reduced and that the small proline-rich proteins and cytokeratins were increased in those derived from HPV 11-infected epithelium compared to healthy genital epithelium. In RNase protection and RT-PCR assays, loricrin transcripts were markedly reduced in HPV 11-infected epithelium compared to uninfected epithelium. Loricrin transcripts were detectable by RNA in situ analysis in isolated cells of HPV 11-infected epithelium, but were absent in large regions of epithelium. We conclude that HPV 11 infection reduces transcription of the loricrin gene and that this leads to a reduction in loricrin incorporation into the CCE. Further studies will examine the effects of specific HPV gene products on transcription of loricrin and other CCE components, as it is likely that viral egress from the infected keratinocyte depends on these effects.

Original languageEnglish
Pages (from-to)240-247
Number of pages8
JournalVirology
Volume298
Issue number2
DOIs
StatePublished - 2002

Fingerprint

Human papillomavirus 11
Epithelium
Proteins
Keratinocytes
loricrin
Papillomavirus Infections
Cellular Structures
Ribonucleases
Keratins
Least-Squares Analysis
Proline
Epidermis
Genes

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

Cite this

Human papillomavirus type 11 alters the transcription and expression of loricrin, the major cell envelope protein. / Lehr, Elizabeth; Jarnik, Michael; Brown, Darron.

In: Virology, Vol. 298, No. 2, 2002, p. 240-247.

Research output: Contribution to journalArticle

@article{34da03d721fa43c4ae39b2a87da15d82,
title = "Human papillomavirus type 11 alters the transcription and expression of loricrin, the major cell envelope protein",
abstract = "Human papillomavirus (HPV) does not induce lysis of infected keratinocytes, and the exact mechanisms of viral escape are not known. As keratinocytes differentiate, the cornified cell envelope (CCE) develops, providing a protective barrier to the host. We previously showed that the normally durable CCE in HPV 11-infected epithelium is fragile compared to CCEs in healthy epithelium. In this study, we examined uninfected and HPV 11-infected human genital epithelium for expression of loricrin, the major CCE protein in healthy epidermis. In HPV 11-infected human genital epithelium, detection of loricrin was reduced in immunoelectron microscopic and immunoblot assays, suggesting that loricrin incorporation into the CCE was reduced or that loricrin synthesis was reduced. Loricrin detection was reduced in immunohistochemical assays in areas of high viral replication. Mathematical modeling by least squares was performed using the amino acid composition of highly purified CCE fragments, confirming that loricrin was markedly reduced and that the small proline-rich proteins and cytokeratins were increased in those derived from HPV 11-infected epithelium compared to healthy genital epithelium. In RNase protection and RT-PCR assays, loricrin transcripts were markedly reduced in HPV 11-infected epithelium compared to uninfected epithelium. Loricrin transcripts were detectable by RNA in situ analysis in isolated cells of HPV 11-infected epithelium, but were absent in large regions of epithelium. We conclude that HPV 11 infection reduces transcription of the loricrin gene and that this leads to a reduction in loricrin incorporation into the CCE. Further studies will examine the effects of specific HPV gene products on transcription of loricrin and other CCE components, as it is likely that viral egress from the infected keratinocyte depends on these effects.",
author = "Elizabeth Lehr and Michael Jarnik and Darron Brown",
year = "2002",
doi = "10.1006/viro.2002.1445",
language = "English",
volume = "298",
pages = "240--247",
journal = "Virology",
issn = "0042-6822",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Human papillomavirus type 11 alters the transcription and expression of loricrin, the major cell envelope protein

AU - Lehr, Elizabeth

AU - Jarnik, Michael

AU - Brown, Darron

PY - 2002

Y1 - 2002

N2 - Human papillomavirus (HPV) does not induce lysis of infected keratinocytes, and the exact mechanisms of viral escape are not known. As keratinocytes differentiate, the cornified cell envelope (CCE) develops, providing a protective barrier to the host. We previously showed that the normally durable CCE in HPV 11-infected epithelium is fragile compared to CCEs in healthy epithelium. In this study, we examined uninfected and HPV 11-infected human genital epithelium for expression of loricrin, the major CCE protein in healthy epidermis. In HPV 11-infected human genital epithelium, detection of loricrin was reduced in immunoelectron microscopic and immunoblot assays, suggesting that loricrin incorporation into the CCE was reduced or that loricrin synthesis was reduced. Loricrin detection was reduced in immunohistochemical assays in areas of high viral replication. Mathematical modeling by least squares was performed using the amino acid composition of highly purified CCE fragments, confirming that loricrin was markedly reduced and that the small proline-rich proteins and cytokeratins were increased in those derived from HPV 11-infected epithelium compared to healthy genital epithelium. In RNase protection and RT-PCR assays, loricrin transcripts were markedly reduced in HPV 11-infected epithelium compared to uninfected epithelium. Loricrin transcripts were detectable by RNA in situ analysis in isolated cells of HPV 11-infected epithelium, but were absent in large regions of epithelium. We conclude that HPV 11 infection reduces transcription of the loricrin gene and that this leads to a reduction in loricrin incorporation into the CCE. Further studies will examine the effects of specific HPV gene products on transcription of loricrin and other CCE components, as it is likely that viral egress from the infected keratinocyte depends on these effects.

AB - Human papillomavirus (HPV) does not induce lysis of infected keratinocytes, and the exact mechanisms of viral escape are not known. As keratinocytes differentiate, the cornified cell envelope (CCE) develops, providing a protective barrier to the host. We previously showed that the normally durable CCE in HPV 11-infected epithelium is fragile compared to CCEs in healthy epithelium. In this study, we examined uninfected and HPV 11-infected human genital epithelium for expression of loricrin, the major CCE protein in healthy epidermis. In HPV 11-infected human genital epithelium, detection of loricrin was reduced in immunoelectron microscopic and immunoblot assays, suggesting that loricrin incorporation into the CCE was reduced or that loricrin synthesis was reduced. Loricrin detection was reduced in immunohistochemical assays in areas of high viral replication. Mathematical modeling by least squares was performed using the amino acid composition of highly purified CCE fragments, confirming that loricrin was markedly reduced and that the small proline-rich proteins and cytokeratins were increased in those derived from HPV 11-infected epithelium compared to healthy genital epithelium. In RNase protection and RT-PCR assays, loricrin transcripts were markedly reduced in HPV 11-infected epithelium compared to uninfected epithelium. Loricrin transcripts were detectable by RNA in situ analysis in isolated cells of HPV 11-infected epithelium, but were absent in large regions of epithelium. We conclude that HPV 11 infection reduces transcription of the loricrin gene and that this leads to a reduction in loricrin incorporation into the CCE. Further studies will examine the effects of specific HPV gene products on transcription of loricrin and other CCE components, as it is likely that viral egress from the infected keratinocyte depends on these effects.

UR - http://www.scopus.com/inward/record.url?scp=0036374958&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036374958&partnerID=8YFLogxK

U2 - 10.1006/viro.2002.1445

DO - 10.1006/viro.2002.1445

M3 - Article

C2 - 12127787

AN - SCOPUS:0036374958

VL - 298

SP - 240

EP - 247

JO - Virology

JF - Virology

SN - 0042-6822

IS - 2

ER -