PMID- 33148169
OWN - NLM
STAT- MEDLINE
DCOM- 20210514
LR  - 20231112
IS  - 1471-2164 (Electronic)
IS  - 1471-2164 (Linking)
VI  - 21
IP  - 1
DP  - 2020 Nov 4
TI  - Differential responses in placenta and fetal thymus at 12 days post infection 
      elucidate mechanisms of viral level and fetal compromise following PRRSV2 
      infection.
PG  - 763
LID - 10.1186/s12864-020-07154-0 [doi]
LID - 763
AB  - BACKGROUND: A pregnant gilt infected with porcine reproductive and respiratory 
      syndrome virus (PRRSV) can transmit the virus to her fetuses across the 
      maternal-fetal-interface resulting in varying disease outcomes. However, the 
      mechanisms leading to variation in fetal outcome in response to PRRSV infection 
      are not fully understood. Our objective was to assess targeted immune-related 
      gene expression patterns and pathways in the placenta and fetal thymus to 
      elucidate the molecular mechanisms involved in the resistance/tolerance and 
      susceptibility of fetuses to PRRSV2 infection. Fetuses were grouped by 
      preservation status and PRRS viral load (VL): mock infected control (CTRL), no 
      virus detected (UNINF), virus detected in the placenta only with viable 
      (PLCO-VIA) or meconium-stained fetus (PLCO-MEC), low VL with viable (LVL-VIA) or 
      meconium-stained fetus (LVL-MEC), and high VL with viable (HVL-VIA) or 
      meconium-stained fetus (HVL-MEC). RESULTS: The host immune response was initiated 
      only in fetuses with detectable levels of PRRSV. No differentially expressed 
      genes (DEG) in either the placenta or thymus were identified in UNINF, PLCO-VIA, 
      and PLCO-MEC when compared to CTRL fetuses. Upon fetal infection, a set of core 
      responsive IFN-inducible genes (CXCL10, IFIH1, IFIT1, IFIT3, ISG15, and MX1) were 
      strongly upregulated in both tissues. Gene expression in the thymus is a better 
      differentiator of fetal VL; the strong downregulation of several innate and 
      adaptive immune pathways (e.g., B Cell Development) are indicative of HVL. Gene 
      expression in the placenta may be a better differentiator of fetal demise than 
      the thymus, based-on principle component analysis clustering, gene expression 
      patterns, and dysregulation of the Apoptosis and Ubiquitination pathways. 
      CONCLUSION: Our data supports the concept that fetal outcome in response to 
      PRRSV2 infection is determined by fetal, and more significantly placental 
      response, which is initiated only after fetal infection. This conceptual model 
      represents a significant step forward in understanding the mechanisms 
      underpinning fetal susceptibility to the virus.
FAU - Van Goor, Angelica
AU  - Van Goor A
AD  - Animal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, 
      ARS, USDA, Beltsville, MD, USA.
FAU - Pasternak, Alex
AU  - Pasternak A
AD  - Department of Animal Sciences, Purdue University, West Lafayette, IN, USA.
AD  - Department of Large Animal Clinical Sciences, Western College of Veterinary 
      Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
FAU - Walker, Kristen
AU  - Walker K
AD  - Animal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, 
      ARS, USDA, Beltsville, MD, USA.
FAU - Hong, Linjun
AU  - Hong L
AD  - College of Animal Science, South China Agricultural University, Guangzhou, China.
FAU - Malgarin, Carolina
AU  - Malgarin C
AD  - Department of Large Animal Clinical Sciences, Western College of Veterinary 
      Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
FAU - MacPhee, Daniel J
AU  - MacPhee DJ
AD  - Department of Veterinary Biomedical Sciences, Western College of Veterinary 
      Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
FAU - Harding, John C S
AU  - Harding JCS
AD  - Department of Large Animal Clinical Sciences, Western College of Veterinary 
      Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
FAU - Lunney, Joan K
AU  - Lunney JK
AUID- ORCID: 0000-0002-1147-8662
AD  - Animal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, 
      ARS, USDA, Beltsville, MD, USA. joan.lunney@usda.gov.
LA  - eng
GR  - project 8042-32000-102/Agricultural Research Service/
GR  - Project 2014LSARP_8202/Genome Canada/
GR  - Project 346143/Genome Prairie/
GR  - Administrative support/Genome Alberta/
GR  - Industry support/PigGen Canada/
PT  - Journal Article
DEP - 20201104
PL  - England
TA  - BMC Genomics
JT  - BMC genomics
JID - 100965258
SB  - IM
MH  - Animals
MH  - Female
MH  - Fetus
MH  - Placenta
MH  - *Porcine Reproductive and Respiratory Syndrome/genetics
MH  - *Porcine respiratory and reproductive syndrome virus
MH  - Pregnancy
MH  - *Pregnancy Complications, Infectious
MH  - Swine
PMC - PMC7640517
OTO - NOTNLM
OT  - Cytokines
OT  - Disease resistance
OT  - Disease susceptibility
OT  - Fetal pig
OT  - Gene expression
OT  - Immunity
OT  - Interferon
OT  - Placenta
OT  - Porcine reproductive and respiratory syndrome
OT  - Thymus
COIS- Dr. Joan Lunney, an author on this manuscript, is a member of the editorial board 
      for the BMC Genomics journal.
EDAT- 2020/11/06 06:00
MHDA- 2021/05/15 06:00
PMCR- 2020/11/04
CRDT- 2020/11/05 05:35
PHST- 2020/07/27 00:00 [received]
PHST- 2020/10/15 00:00 [accepted]
PHST- 2020/11/05 05:35 [entrez]
PHST- 2020/11/06 06:00 [pubmed]
PHST- 2021/05/15 06:00 [medline]
PHST- 2020/11/04 00:00 [pmc-release]
AID - 10.1186/s12864-020-07154-0 [pii]
AID - 7154 [pii]
AID - 10.1186/s12864-020-07154-0 [doi]
PST - epublish
SO  - BMC Genomics. 2020 Nov 4;21(1):763. doi: 10.1186/s12864-020-07154-0.