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Title:The effects of maternal and postnatal infections with porcine reproductive and respiratory virus on muscle growth and development in piglets
Author(s):Clark, Diana
Advisor(s):Dilger, Anna C.
Department / Program:Animal Sciences
Discipline:Animal Sciences
Degree Granting Institution:University of Illinois at Urbana-Champaign
Degree:M.S.
Genre:Thesis
Subject(s):Porcine Reproductive and Respiratory Syndrome Virus
Muscle Growth
Muscle Development
Postnatal Infection
Prenatal Infection
Abstract:Infection can reduce feed intake, limit weight gain, and decrease muscle growth by directing nutrients away from protein accretion and towards an inflammatory response; however, it is unclear how maternal infection affects offspring skeletal muscle development. Additionally, it is unclear how viral infections mechanistically reduce skeletal muscle growth and protein accretion. Pregnant gilts were inoculated with PRRSV (P piglets) or sterile culture medium (C Piglets) at 80 days of gestation. Offspring were euthanized at birth (d0) or at four weeks of age (d28). Samples from the longissimus dorsi (LD) and psoas major (PM) were used for gene expression, while the semitendinosus (ST) at d28 was used to determine muscle fiber area and number. At d0 relative LD weight was decreased (P=0.01) while PM was increased (P=0.01) in P piglets compared with C piglets. At d28, whole LD (P=0.01) and relative LD weight (P=0.03) decreased in P piglets compared with C piglets. Cell number decreased (P=0.04) while muscle fiber cross sectional area within ST increased (P=0.02) in P piglets compared with C piglets. At d0 in the LD, maternal PRRSV infection resulted in a shift towards more oxidative fiber type expression and a decrease in negative growth factors as myosin heavy chain (MHC) 2b (P=0.02), MHC2x (P=0.01), and myostatin (P=0.01) expression decreased in P piglets compared with C piglets. However, at d28, there were no differences in MHC expression. A shift towards more oxidative fiber types also occurred in the PM at d0, as MHC1 expression was increased (P=0.03) in P piglets compared with C piglets. Furthermore, an increase in positive growth factors was observed as myogenic differentiation 1 (P<0.01) and myogenin (P<0.01) increased while myostatin expression decreased (P=0.04) in P piglets compared with C piglets. These data suggest maternal PRRSV infection restricts in utero muscle fiber development. Postnatal infection was evaluated in pigs inoculated with PRRSV or sterile culture medium (control) at 35 days of age. Pigs were maintained on similar diets and euthanized at 49 days of age. Samples from the LD and PM were used for gene expression, while the ST was used to determine muscle fiber cross sectional area and number. From 35 to 49 days of age, body weight gain (P<0.01) and feed intake (P<0.04) were reduced in PRRSV inoculated pigs compared with control pigs. However, feed to gain ratio was only reduced (P<0.01) the first week after inoculation in PRRSV inoculated pigs compared with control. Longissimus dorsi and ST weights were decreased (P<0.01) and relative PM weight was reduced (P<0.01) in pigs inoculated with PRRSV compared with control pigs. In addition, muscle fiber size of PRRSV inoculated pigs tended to be reduced (P=0.09) compared with control pigs, but muscle cell number was unaffected. In the PM, myostatin expression tended to be increased (P=0.08) while myogenic factor 5 (P=0.01) and insulin-like growth factor 1 (P=0.04) were decreased in pigs inoculated with PRRSV compared with control pigs. Infection had minimal effects on myogenic growth factors in the LD as myogenic differentiation factor 1 (MYOD) was increased (P<0.01) and IGF 2 was decreased (P=0.04) in pigs inoculated with PRRSV compared with control pigs. Porcine reproductive and respiratory virus infection decreased muscle weights and cell size through a decrease in myogenic growth factor expression. However, differences between muscles suggest muscles may respond differently to PRRSV infection depending on their fiber type composition.
Issue Date:2015-01-21
URI:http://hdl.handle.net/2142/72889
Rights Information:Copyright 2014 Diana Clark
Date Available in IDEALS:2015-01-21
Date Deposited:2014-12


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