Swine coronaviruses include the following six members, namely porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis virus (TGEV), porcine delta coronavirus (PDCoV), swine acute diarrhea syndrome coronavirus (SADS-CoV), porcine hemagglutinating encephalomyelitis virus (PHEV), and porcine respiratory coronavirus (PRCV). Clinically, PEDV, TGEV, PDCoV, and SADS-CoV cause enteritis, whereas PHEV induces encephalomyelitis, and PRCV causes respiratory disease. Years of studies reveal that swine coronaviruses replicate in the cellular cytoplasm exerting a wide variety of effects on cells. Some of these effects are particularly pertinent to cell pathology, including endoplasmic reticulum (ER) stress, unfolded protein response (UPR), autophagy, and apoptosis. In addition, swine coronaviruses are able to induce cellular changes, such as cytoskeletal rearrangement, alterations of junctional complexes, and epithelial-mesenchymal transition (EMT), that render enterocytes unable to absorb nutrients normally, resulting in the loss of water, ions, and protein into the intestinal lumen. This review aims to describe the cellular changes in swine coronavirus-infected cells and to aid in understanding the pathogenesis of swine coronavirus infections. This review also explores how the virus exerted subcellular and molecular changes culminating in the clinical and pathological findings observed in the field.

Porcine epidemic diarrhea virus (PEDV) infection leads to diarrhea and subsequently to decreased feed efficiency and growth in weaned pigs. Given that few studies have addressed the host-virus interaction in vivo, this study focused on endoplasmic reticulum (ER) stress and unfolded protein response (UPR) in jejunal epithelial cells during PEDV infection. Eight-week-old pigs (n = 64) were orally inoculated with PEDV IN19338 strain (n = 40) or sham-inoculated (n = 24) and analyzed for PEDV viral RNA shedding using reverse transcription–quantitative polymerase chain reaction and for viral antigen within enterocytes using immunohistochemistry (IHC). ER stress was analyzed in a subset of 9 PEDV-inoculated pigs with diarrhea, detectable viral RNA, and viral antigen (PEDV-immunopositive pigs). Compared with control pigs, PEDV-immunopositive pigs had a reduced ratio of villus height to crypt depth in the jejunum (P = .002, n = 9 per group), consistent with intestinal injury. The protein levels of ATF6, IRE1, PERK, XBP1u, ATF4, GRP78, and caspase-3 were assessed in jejunal epithelial cells at the villus tips via IHC. Both ER stress and UPR were demonstrated in PEDV-immunopositive pigs by the increased expression of ATF6 (P = .047), IRE1 (P = .007), and ATF4 (P = .001). The expression of GRP78 (P = .024) and caspase-3 (P = .004) were also increased, indicating an accompanying increase in ER protein folding capacity and apoptosis. Overall, these results reveal that PEDV infection induces ER stress and UPR in intestinal epithelial cells of weaned pigs.

In the small intestine, localized innate mucosal immunity is critical for intestinal homeostasis. Porcine epidemic diarrhea virus (PEDV) infection induces villus injury and impairs digestive function. Moreover, the infection might comprise localized innate mucosal immunity. This study investigated specific enterocyte subtypes and innate immune components of weaned pigs during PEDV infection. Four-week-old pigs were orally inoculated with PEDV IN19338 strain (n = 40) or sham-inoculated (n = 24). At day post inoculation (DPI) 2, 4, and 6, lysozyme expression in Paneth cells, cellular density of villous and Peyer’s patch microfold (M) cells, and the expression of polymeric immunoglobulin receptor (pIgR) were assessed in the jejunum and ileum by immunohistochemistry, and interleukin (IL)-1β and tumor necrosis factor (TNF)-α were measured in the jejunum by ELISA. PEDV infection led to a decrease in the ratios of villus height to crypt depth (VH–CD) in jejunum at DPI 2, 4, and 6 and in ileum at DPI 4. The number of villous M cells was reduced in jejunum at DPI 4 and 6 and in ileum at DPI 6, while the number of Peyer’s patch M cells in ileum increased at DPI 2 and then decreased at DPI 6. PEDV-infected pigs also had reduced lysozyme expression in ileal Paneth cells at DPI 2 and increased ileal pIgR expression at DPI 4. There were no significant changes in IL-1β and TNF-α expression in PEDV-infected pigs compared to controls. In conclusion, PEDV infection affected innate mucosal immunity of weaned pigs through alterations in Paneth cells, villous and Peyer’s patch M cells, and pIgR expression.

The coccidian Eimeria necatrix infects the mid-intestine of chickens, causing hemorrhage and resulting in significant economic losses. However, there is a lack of a clear method for evaluating the tissue lesions caused by E. necatrix infection. Moreover, the impact of E. necatrix infection on gut microbiota and metabolites remains to be explored. Therefore, this study was conducted to investigate the effects of E. necatrix infection on the intestinal tissues of chickens and establish a novel histopathological scoring system for evaluating lesion severity. In addition, changes in gut microbiota and metabolites after E. necatrix infection were evaluated. Chickens aged 3 weeks were divided into 5 groups (4 experimental groups and a control group), with 6 chickens in each group. The experimental groups were orally inoculated with different concentrations of E. necatrix oocysts. Intestinal and fecal samples were collected on 7 days post-infection (DPI) and analyzed. Chickens infected with a high dose of E. necatrix exhibited diarrhea, bloody stools, and partial mortality within 6 DPI. Pathological analysis revealed a remarkable reduction in villous height, along with severe hemorrhage, necrosis, and inflammation. The histopathological scoring system revealed a strong correlation with other disease-related indicators, such as weight loss and oocyst shedding, demonstrating its stability and accuracy. Furthermore, the severity of villous lesions was closely associated with alterations in gut microbiota composition. Microbiota analysis showed a considerable reduction in the abundance of Lactobacillus in the high-dose group, whereas the abundance of potential pathogenic bacteria, including Shigella and Escherichia coli, increased, causing gut dysbiosis. Finally, metabolomic analysis indicated that E. necatrix infection disrupted energy and amino acid metabolism, particularly affecting glycolysis, the tricarboxylic acid cycle, and pyruvate metabolism. Overall, this study establishes a reliable histopathological scoring method and confirms that E. necatrix infection causes gut dysbiosis and metabolic abnormalities through tissue damage. These data provide novel insights into the diagnosis and treatment of coccidiosis in chickens.

Compared to the number of studies on the neoplasms of laboratory rodents, fewer studies have focused on spontaneous neoplasms in pet rodents. Notably, the mouse mammary tumor virus (MMTV) is associated with mammary tumors in rodents. In this study, 77 tumors and tumor-like lesions of biopsy samples were collected from 70 pet rodents, including hamsters (n = 47), guinea pigs (n = 16), unknown species (n = 4), rats (n = 2), and a gerbil. Fifty tumors were collected from 47 hamsters, in which the most common tumors were mammary tumors (13/50), followed by fibrosarcoma (9/50), mast cell tumors (4/50), and squamous cell carcinoma (4/50). The collected subtypes of mammary tumors in hamsters included tubular carcinoma (n = 5), tubular adenoma (n = 4), carcinoma and malignant myoepithelioma (n = 1), simple tubular carcinoma (n = 1), adenosquamous carcinoma (n = 1), and tubulopapillary adenoma (n = 1). In addition, twenty tumors were collected from guinea pigs, in which the most common tumor was lipoma (6/20), followed by adenocarcinoma of the mammary gland (4/20), trichofolliculoma (2/20), and collagenous hamartomas (2/20). In guinea pigs, the subtypes of mammary gland tumors were tubular carcinoma (n = 2), tubular and solid carcinoma (n = 1), and tubulopapillary carcinoma (n = 1). In 20 cases of mammary tumors, MMTV was not detected, implicating no evidence of MMTV infection in mammary oncogenesis in pet rodents in Taiwan.