PMID- 23341859
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130124
LR  - 20220318
IS  - 1874-3579 (Electronic)
IS  - 1874-3579 (Linking)
VI  - 6
DP  - 2012
TI  - The immune response to papillomavirus during infection persistence and 
      regression.
PG  - 241-8
LID - 10.2174/1874357901206010241 [doi]
AB  - Human papillomavirus (HPV) infections cause a significant global health burden, 
      predominantly due to HPV-associated cancers. HPV infects only the epidermal cells 
      of cutaneous and mucosal skin, without penetration into the dermal tissues. 
      Infections may persist for months or years, contributed by an array of viral 
      immune evasion mechanisms. However in the majority of cases immunity-based 
      regression of HPV lesions does eventually occur. The role of the innate immune 
      response to HPV in persistence and regression of HPV infection is not well 
      understood. Although an initial inflammatory infiltrate may contribute to disease 
      regression, sustained inflammation at the HPV-induced lesions, characterized by 
      macrophage and neutrophil infiltration, has been observed in persistence. 
      Pathogen-associated molecular patterns (PAMPs) are important in innate 
      recognition. The double stranded DNA and an L1 and L2 capsid components of the 
      HPV virion are potential PAMPs that can trigger signaling through cellular 
      pattern recognition receptors, including toll-like receptors (TLR). TLR 
      expression is increased in regressing HPV disease but is reduced in persistent 
      lesions, suggesting a role for TLR in HPV regression. With regard to the adaptive 
      immune response, a key indicator of regression in humans is infiltration of the 
      lesion with both CD4 and CD8 T cells. In individuals with persistent lesions, CD8 
      T cell and immune suppressive regulatory T cells (Tregs) infiltrate the infection 
      site. There is no association between persistence or regression and the presence 
      of serum antibodies to the viral capsid antigens of HPV. There is still much to 
      be learned about the immunological events that trigger regression of HPV disease. 
      Understanding the viral and host factors that influence persistence and 
      regression is important for the development of better immunotherapeutic 
      treatments for HPV-associated disease.
FAU - Hibma, Merilyn H
AU  - Hibma MH
AD  - Department of Microbiology and Immunology, University of Otago, P.O. Box 56, 
      Dunedin, New Zealand.
LA  - eng
PT  - Journal Article
DEP - 20121228
PL  - United Arab Emirates
TA  - Open Virol J
JT  - The open virology journal
JID - 101480213
PMC - PMC3547310
OTO - NOTNLM
OT  - Adaptive immunity
OT  - epidermis
OT  - immune evasion
OT  - innate immunity
OT  - papillomavirus
OT  - persistence
OT  - regression.
EDAT- 2013/01/24 06:00
MHDA- 2013/01/24 06:01
PMCR- 2012/01/01
CRDT- 2013/01/24 06:00
PHST- 2012/04/30 00:00 [received]
PHST- 2012/08/29 00:00 [revised]
PHST- 2012/09/03 00:00 [accepted]
PHST- 2013/01/24 06:00 [entrez]
PHST- 2013/01/24 06:00 [pubmed]
PHST- 2013/01/24 06:01 [medline]
PHST- 2012/01/01 00:00 [pmc-release]
AID - TOVJ-6-241 [pii]
AID - 10.2174/1874357901206010241 [doi]
PST - ppublish
SO  - Open Virol J. 2012;6:241-8. doi: 10.2174/1874357901206010241. Epub 2012 Dec 28.