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COVID-19 is a new respiratory illness caused by SARS-CoV-2, and has constituted a global public health emergency. Cat is susceptible to SARS-CoV-2. However, the prevalence of SARS-CoV-2 in cats remains largely unknown. Here, we investigated the infection of SARS-CoV-2 in cats during COVID-19 outbreak in Wuhan by serological detection methods. A cohort of serum samples were collected from cats in Wuhan, including 102 sampled after COVID-19 outbreak, and 39 prior to the outbreak. Fifteen sera collected after the outbreak were positive for the receptor binding domain (RBD) of SARS-CoV-2 by indirect enzyme linked immunosorbent assay (ELISA). Among them, 11 had SARS-CoV-2 neutralizing antibodies with a titer ranging from 1/20 to 1/1080. No serological cross-reactivity was detected between SARS-CoV-2 and type I or II feline infectious peritonitis virus (FIPV). In addition, we continuously monitored serum antibody dynamics of two positive cats every 10 days over 130 days. Their serum antibodies reached the peak at 10 days after first sampling, and declined to the limit of detection within 110 days. Our data demonstrated that SARS-CoV-2 has infected cats in Wuhan during the outbreak and described serum antibody dynamics in cats, providing an important reference for clinical treatment and prevention of COVID-19.

Feline infectious peritonitis (FIP) is caused by infection with the feline coronavirus (FCoV) and is fatal if left untreated. In most cats, FCoV primarily infects the gastrointestinal tract and remains asymptomatic or causes only mild enteritis, with only a small proportion of infected cats developing FIP. An excessive and harmful immune response leading to characteristic (pyo)granulomatous phlebitis is believed to play a key role in the development of FIP, along with complex interactions between host and viral factors. Our research group recently demonstrated successful treatment of cats with naturally occurring FIP using the antiviral nucleoside analogue GS-441524. Treatment led to complete recovery without any relapses for a follow-up period of one year, demonstrating both a short- and long-term cure. To investigate differential gene expression and corresponding molecular pathways in cats with FIP before, during, and after antiviral treatment, RNA sequencing was performed on full blood samples of 18 cats treated successfully in a prospective study. Samples were analyzed before treatment, at different timepoints while on treatment with GS-441524 and after completion of treatment. Additionally, gene expression profiles were compared to 12 healthy FCoV-infected control cats and 5 healthy uninfected control cats. The results revealed both a widespread dysregulation of the blood RNA signature in cats with FIP as well as its rapid normalization within the first week of treatment. Significant changes were already apparent within the first two days of treatment. The results of the present study suggest that elimination of the virus from the blood leads to rapid control and subsequent normalization of the damaging immune response, a finding that corresponds well to the clinical response to treatment. This study illustrates the host response to treatment at the molecular level and provides further evidence that a shorter treatment duration than the 84 days predominantly practiced is sufficient.

Feline coronaviruses (FCoVs) are divided into two groups: feline infectious peritonitis virus (FIPV) and feline enteric coronavirus (FECV). FIPV is responsible for the severe disease known as feline infectious peritonitis, while FECV typically causes mild symptoms, such as diarrhea, and often does not lead to any disease at all. Currently, it is not possible to distinguish between FIPV and FECV at the molecular level. Therefore, there is an urgent need to understand the molecular features of FIPV. Here, we generated a recombinant virus by replacing the ORF1ab region and the coding sequence for the spike (S) protein of an FECV with the corresponding sequences from FIPVs. The recombinant virus (recFECV-SDF-2-1abFIPV) exhibited similar growth kinetics to its parental strain. Our analysis revealed that the replacement of the ORF1ab in the FECV caused significant alterations in protein expression within the host cells. Furthermore, the presence of the ORF1ab from the FIPV strain resulted in enhanced suppression of the innate immune response compared to the parental strain, as determined through proteomic and transcriptomic studies. Additionally, we demonstrated that the papain-like protease 2 (PL2pro) of the non-structural protein 3 (NSP3) from both FIPV and FECV functions in immune suppression, and the protease activity is required for this function.

Feline infectious peritonitis (FIP) is a fatal disease in cats caused by infection with feline coronavirus (FCoV). Despite severe inflammatory changes, defense mechanisms fail to achieve virus clearance. Some studies focused on various immune evasion mechanisms, but none of these studies elucidated the inefficacy of the complement system, which is one major player in FIP-associated immune pathogenesis. This study aimed to investigate the involvement of complement-regulating factors (CRFs). CRFs help modulate the immune response and prevent host tissue damage. Archived tissue samples from 31 deceased, FIP-affected cats were evaluated using multiplex immunohistochemistry for the spatial expression of the complement-regulating factors CD46 and CD59 in association with FIP lesions and their colocalization with complement-activating factor C1q and membrane attack complex C9 in relation to the presence and proximity of FCoV-infected cells. The FIP lesions of all 31 cats exhibited marked expression of both complement-regulating factors in proximity to FCoV-infected macrophages. Moreover, their expression in all 31 animals was significantly lower than the expression of the complement-activating factors C1q and C9 compared to areas farther distal to FCoV-infected cells. In conclusion, FCoV-infected macrophages in cats with FIP appear to use autocrine and paracrine expression of complement-regulating factors in their immediate environment to shield themselves from destruction by the complement system.

Currently, there is no effective vaccine against feline coronavirus infections. The coronavirus Spike (S) protein plays a critical role in viral binding to cell receptors and contains multiple neutralizing antibody epitopes that trigger the host's immune response to combat infection. Selecting an optimized adjuvant is essential to ensure robust vaccine-induced immunity against pathogenic infections. To produce a recombinant S protein for the development of subunit vaccines and evaluate the immune responses elicited by different adjuvants. In this study, we developed three subunit vaccines incorporating distinct adjuvants: Alh, ISA201, and CFA FCoV-SP. BALB/c mice were immunized three times via subcutaneous injections with each vaccine formulation. Serum samples were then analyzed to evaluate S protein-specific IgG levels and cytokine concentrations using enzyme-linked immunosorbent assay (ELISA), assessing the magnitude and nature of the vaccine-induced immune responses. The ISA201 FCoV-SP vaccine induced significantly higher total IgG levels than those in the Alh or CFA groups. All tested protein concentrations resulted in increased serum IgG antibody levels, with the optimal immune dose of recombinant S protein being 15 µg/dose. Additionally, the ISA201 FCoV-SP vaccine led to increased expression of interferon-γ, interleukin-8, and tumor necrosis factor-α. Collectively, our findings suggest that ISA201 serves as the most effective adjuvant for a recombinant S protein subunit vaccine against FCoV. Additionally, the subunit vaccine developed in this study exhibited acceptable immune responses in mice.

Feline coronavirus (FCoV) is a pathogenic virus commonly found in cats that causes a benign enteric illness and fatal systemic disease, feline infectious peritonitis. The development of serological diagnostic tools for FCoV is helpful for clinical diagnosis and epidemiological investigation. Therefore, this study aimed to develop an indirect enzyme-linked immunosorbent assay (iELISA) to detect antibodies against FCoV using histidine-tagged recombinant spike protein. FCoV S protein (1127–1400 aa) was expressed and used as an antigen to establish an ELISA. Mice and rabbits immunized with the protein produced antibodies that were recognized and bound to the protein. The intra-assay coefficient of variation (CV) was 1.15–5.04% and the inter-assay CV was 4.28–15.13%, suggesting an acceptable repeatability. iELISA did not cross-react with antisera against other feline viruses. The receiver operating characteristic curve analysis revealed an 86.7% sensitivity and 93.3% specificity for iELISA. Serum samples (n = 107) were tested for anti-FCoV antibodies, and 70.09% of samples were positive for antibodies against FCoV. The iELISA developed in our study can be used to measure serum FCoV antibodies due to its acceptable repeatability, sensitivity, and specificity. Additionally, field sample analysis data demonstrated that FCoV is highly prevalent in cat populations in Fujian province, China.

Feline coronavirus (FCoV) has been classified into two biotypes: avirulent feline coronavirus (feline enteric coronavirus: FECV) and virulent feline coronavirus (feline infectious peritonitis virus: FIPV). In FIPV infection, antibody-dependent enhancement (ADE) has been reported and was shown to be associated with severe clinical disease. On the other hand, the potential role of ADE in FECV infection has not been examined. In this study, using laboratory strains of serotype II FIPV WSU 79-1146 (FIPV 79-1146) and serotype II FECV WSU 79-1683 (FECV 79-1683), we investigated the relationship between ADE and induction of inflammatory cytokines, which are pathogenesis-related factors, for each strain. As with ADE of FIPV 79-1146 infection, a monoclonal antibody against the spike protein of FCoV (mAb 6-4-2) enhanced FECV 79-1683 replication in U937 cells and primary feline monocytes. However, the ADE activity of FECV 79-1683 was lower than that of FIPV 79-1146. Moreover, mRNA levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6) significantly increased with ADE of FIPV 79-1146 infection in primary feline monocytes, but FECV 79-1683 did not demonstrate an increase in these levels. In conclusion, infection of monocytes by FECV was enhanced by antibodies, but the efficiency of infection was lower than that of FIPV.

Feline infectious peritonitis (FIP) is caused by mutated feline coronaviruses. Immune-mediated hemolytic anemia (IMHA) arises due to immune-mediated erythrocyte destruction and can be non-associative or associative with diseases such as FIP. Records of cats with FIP were reviewed to find those with associative IMHA based on exclusion of other causes of anemia and a positive saline agglutination test and/or Coombs test. The inclusion criteria were met for 45 cats (26 (58%) cats with effusive and 19 (42%) with non-effusive FIP). Median hematocrit was 18% (interquartile range [IQR] 13–20). Anemia was non-regenerative in 36 (80%) cats and regenerative in 5 (11%) cats; 4 (9%) cats had no reticulocyte count available. Concurrent thrombocytopenia was present in 18 (40%) cats. All 45 cats were treated with nucleoside analogs, and 44 (98%) cats with glucocorticoids; in 5 (11%) cats, glucocorticoids were added after starting antiviral treatment due to persistent anemia. Median follow-up was 72 days (IQR 14–246); at the time of last follow-up 33 (73%) cats had survived while 12 (27%) had died or were euthanized. Of the 33 surviving cats, 17 achieved remission of both FIP and IMHA. In three cats, FIP remission was achieved, but IMHA relapsed; in one of these, IMHA relapsed twice. FIP relapsed without IMHA in two cats, and both FIP and IMHA relapsed in one cat. In 9 cats the antiviral and glucocorticoid treatment is still ongoing at the time of the publication. Although FIP is likely an uncommon cause of associative IMHA, as more cats with FIP are treated with antiviral therapy, it is important to consider IMHA as a possible cause of anemia in cats with FIP.

ABSTRACT Background Understanding the nature of inflammatory responses in cats with bacterial and viral infections is essential for accurately managing the infection. This study aimed to investigate the diversities of inflammatory responses between bacterial and viral infections in cats to figure out their role in the pathophysiology of these infections. Methods Seventy‐five owned cats were included in the study. The evaluations were performed based on three groups: healthy control, bacterial infection group (those with bronchopneumonia and gastrointestinal tract and urinary tract infections) and viral infection group (21 with feline coronavirus [FCoV], 3 with feline leukaemia virus [FeLV] and 1 with feline calicivirus), each containing 25 individuals. Total and differential leukocyte counts, C‐reactive protein (CRP), transforming growth factor beta (TGF‐β), interleukin‐6 (IL‐6), tumour necrosis factor‐alpha (TNF‐α), interleukin‐1 beta (IL‐1β) and interleukin‐10 (IL‐10) concentrations were assessed in the blood samples collected from sick and healthy animals. Results No statistically significant difference was noted in serum TNF‐α, IL‐1β and IL‐10 concentrations of the infected cats (p = 0.996, p = 0.160 and p = 0.930, respectively). Serum TGF‐β concentration in the viral infection group was reduced compared to the healthy control (p = 0.001). In contrast, WBC count and IL‐6 and CRP concentrations were increased in the cats with bronchopneumonia, gastrointestinal tract infections and urinary tract infections compared to the healthy control and viral infection groups (p = 0.001, p = 0.001 and p = 0.001, respectively). Conclusion This study revealed significant differences between bacterial and viral infections regarding the fashion of inflammatory responses in cats, and the relevant data will undoubtedly contribute to the management and control of feline infectious diseases, rendering the development of novel therapeutic strategies. This study investigates the differences in inflammatory responses between bacterial and viral infections in cats, which is crucial for effective infection management. We included 75 cats divided into three groups: healthy controls, bacterial infections (bronchopneumonia, gastrointestinal and urinary tract infections) and viral infections. Key findings include significantly reduced serum TGF‐β in viral infections compared to healthy controls and increased WBC count, IL‐6 and CRP in cats with bacterial infections. No significant differences were found for TNF‐α, IL‐1β and IL‐10. These results highlight distinct inflammatory response patterns between bacterial and viral infections, which may guide better management and treatment strategies for feline infectious diseases.

Coronavirus frequently infects humans and animals, showing the ability to recombine and cross over to different species. Cats can be considered a model for studying coronavirus infection, in which feline coronavirus (FCoV) represents a major enteric pathogen related to gastroenteric disease. In this animal, the virus can acquire tropism for macrophage cells, leading to a deadly disease called feline infectious peritonitis (FIP). In this study, monocyte-derived macrophages were isolated by CD14-positive selection in venous whole blood from 26 cats with FIP and 32 FCoV-positive healthy cats. Phagocytosis and respiratory burst activities were investigated and compared between the groups. This is the first study comparing macrophage activity in cats affected by FIP and healthy cats positive for FCoV infection. Our results showed that in cats with FIP, the phagocytic and respiratory burst activities were significantly lower. Our results support the possible role of host immunity in Coronaviridae pathogenesis in cats, supporting future research on the immune defense against this systemic disease.