PMID- 19594394
OWN - NLM
STAT- MEDLINE
DCOM- 20090916
LR  - 20191210
IS  - 1557-8976 (Electronic)
IS  - 0882-8245 (Linking)
VI  - 22
IP  - 4
DP  - 2009 Jul
TI  - Antimicrobial host defense peptides in an arteriviral infection: differential 
      peptide expression and virus inactivation.
PG  - 235-42
LID - 10.1089/vim.2009.0005 [doi]
AB  - Antimicrobial host defense peptides (AHDPs) are effective against a wide range of 
      microbes, including viruses. The arteriviral infection caused by porcine 
      reproductive and respiratory syndrome virus (PRRSV) is a devastating pandemic 
      that causes the most economically significant disease of swine. We sought to 
      determine if the expression of AHDPs was influenced by infection with PRRSV, and 
      if porcine AHDPs have direct antiviral activity against PRRSV. Because pulmonary 
      alveolar macrophages (PAMs) are primary targets of PRRSV infection, gene 
      expression of porcine AHDPs was evaluated in lungs from fetal and 2-wk-old 
      congenitally infected pigs. In PRRSV-positive lungs and PAMs, gene expression of 
      most porcine AHDPs showed little upregulation. However, gene expression of 
      porcine beta-defensin-1 (pBD-1), pBD-4, pBD-104, pBD-123, and pBD-125 were 
      downregulated more than threefold in 2-wk-old congenitally infected pig lungs. 
      Incubation of PRRSV with pBD-3 or PG-4 significantly inhibited viral infectivity 
      in MARC-145 cells. Using nine protegrin or protegrin-derived peptides, we 
      determined that a cyclic analog of PG-4 increased anti-PRRSV activity, and that 
      substitution of phenylalanine with valine eliminated most PG-4 antiviral 
      activity. In PAMs, pBD-3 and PG-4 at 5-40 microg/mL consistently suppressed PRRSV 
      titers. Collectively, these findings suggest a potential role for some porcine 
      AHDPs as innate antiviral effectors in PRRSV infection. Moreover, modulation of 
      porcine innate immune mechanisms with AHDPs may be one means of limiting the 
      impact of this costly pandemic viral disease.
FAU - Sang, Yongming
AU  - Sang Y
AD  - Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas 
      State University, Manhattan, Kansas 66506-5802, USA.
FAU - Ruchala, Piotr
AU  - Ruchala P
FAU - Lehrer, Robert I
AU  - Lehrer RI
FAU - Ross, Chris R
AU  - Ross CR
FAU - Rowland, Raymond R R
AU  - Rowland RR
FAU - Blecha, Frank
AU  - Blecha F
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Viral Immunol
JT  - Viral immunology
JID - 8801552
RN  - 0 (Anti-Infective Agents)
RN  - 0 (Antimicrobial Cationic Peptides)
RN  - 0 (beta-Defensins)
RN  - 157214-61-4 (protegrin-4)
RN  - 63231-63-0 (RNA)
SB  - IM
MH  - Animals
MH  - Anti-Infective Agents/pharmacology
MH  - Antimicrobial Cationic Peptides/biosynthesis/immunology/pharmacology
MH  - Cell Line
MH  - Chlorocebus aethiops
MH  - Female
MH  - Gene Expression Regulation/immunology
MH  - Lung/metabolism
MH  - Macrophages, Alveolar/metabolism
MH  - *Porcine Reproductive and Respiratory Syndrome/immunology/metabolism
MH  - Porcine respiratory and reproductive syndrome virus/drug 
      effects/pathogenicity/physiology
MH  - RNA/analysis/biosynthesis/genetics
MH  - Swine
MH  - Virulence
MH  - Virus Inactivation/*drug effects
MH  - beta-Defensins/*biosynthesis/immunology/pharmacology
EDAT- 2009/07/15 09:00
MHDA- 2009/09/17 06:00
CRDT- 2009/07/15 09:00
PHST- 2009/07/15 09:00 [entrez]
PHST- 2009/07/15 09:00 [pubmed]
PHST- 2009/09/17 06:00 [medline]
AID - 10.1089/vim.2009.0005 [doi]
PST - ppublish
SO  - Viral Immunol. 2009 Jul;22(4):235-42. doi: 10.1089/vim.2009.0005.