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Review
. 2023 Jan 27;15(2):359.
doi: 10.3390/v15020359.

Transmissible Gastroenteritis Virus: An Update Review and Perspective

Yiwu Chen  1 , Yuanzhu Zhang  1 , Xi Wang  1 , Jian Zhou  1 , Lerong Ma  1 , Jianing Li  1 , Lin Yang  1 , Hongsheng Ouyang  1   2   3 , Hongming Yuan  1   2 , Daxin Pang  1   2   3
Affiliations
Review

Transmissible Gastroenteritis Virus: An Update Review and Perspective

Yiwu Chen et al. Viruses. .

Abstract

Transmissible gastroenteritis virus (TGEV) is a member of the alphacoronavirus genus, which has caused huge threats and losses to pig husbandry with a 100% mortality in infected piglets. TGEV is observed to be recombining and evolving unstoppably in recent years, with some of these recombinant strains spreading across species, which makes the detection and prevention of TGEV more complex. This paper reviews and discusses the basic biological properties of TGEV, factors affecting virulence, viral receptors, and the latest research advances in TGEV infection-induced apoptosis and autophagy to improve understanding of the current status of TGEV and related research processes. We also highlight a possible risk of TGEV being zoonotic, which could be evidenced by the detection of CCoV-HuPn-2018 in humans.

Keywords: TGEV; TGEV variant strains; TGEV virulence; alphacoronavirus; zoonotic.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Schematic diagram of the TGEV genome structure. Non-structural proteins, including ORF1a and 1b, ORF3a/3b and ORF7; structural proteins, including spike (S), envelope (E), membrane (M), and nucleocapsid (N) proteins. S protein is used to divide different TGEV subtypes: (a) nt1123–1128 deletion of the S protein is considered to be Purdue strain; (b) ORF3 nt−75–−60 and nt195–223 deletions (between S protein and ORF 3) are considered to be Miller subtypes; (c) and TGEV with a deletion of nt621–681 in S protein is variant strain PRCV and infects the porcine respiratory tract.
Figure 2
Figure 2
Diagram of the roles of apoptosis in the TGEV infection.
Figure 3
Figure 3
Schematic diagram of the role of autophagy in TGEV in infected host cells. TGEV infects host cell through the S protein recognition receptor pAPN, and this process can also be achieved by the non-protein receptor sialic acid. Then, it is entered and released through the endosomal pathway. Nsp3 and Nsp4 are hydrolyzed and bound to the endoplasmic reticulum, hijacking the host endoplasmic reticulum and recruiting TMEM41B and VMP1 to form the membrane vesicles necessary for viral replication, a process that may involve Nsp6.
See this image and copyright information in PMC

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