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Porcine transmissible gastroenteritis virus (TGEV) is an enveloped, positive-sense, single-stranded RNA virus belonging to the genus Alphacoronavirus within the family Coronaviridae [7, 10]. It is the causative agent of transmissible gastroenteritis (TGE), a highly contagious and devastating enteric disease in swine characterized by severe diarrhea, vomiting, and dehydration [11, 14]. The virus primarily infects the mature villous enterocytes of the small intestine, leading to significant villous atrophy and malabsorption [11, 13]. TGEV enters host cells through the interaction of its Spike (S) protein with the porcine aminopeptidase N (pAPN) receptor [5, 7]. While vaccines are available, there are currently no specific antiviral drugs approved for clinical use in pigs, making the development of inhibitors targeting the viral main protease (3CLpro) and RNA-dependent RNA polymerase (RdRp) a priority in veterinary research [1, 3, 13]. The virus poses a major economic threat to the global pork industry due to its near 100% mortality rate in neonatal piglets [1, 2, 10]. Experimental treatments have explored the use of small molecules like phloretin and ribavirin to inhibit viral replication and assembly [2, 6]. Additionally, host-targeted strategies such as inhibiting serine proteases like TMPRSS2 have shown potential in blocking viral entry [6]. Understanding the molecular mechanisms of TGEV pathogenesis and immune evasion is crucial for developing more effective control measures [9, 17]. The virus also serves as a model for studying coronavirus biology and cross-species transmission risks [10, 12].
Inhibition of viral main protease (3CLpro), inhibition of RNA-dependent RNA polymerase (RdRp), inhibition of viral entry via Spike protein targeting, and inhibition of host cell serine proteases such as TMPRSS2.
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