Q: In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
are lacking, the present study investigated these missing links during experimental infection of three SPF cats with FECV strain UCD. Two cats showed mild clinical signs, faecal shedding of infectious virus from 4 dpi, a cell-associated viraemia at inconsistent time points from 5 dpi, a highly neutralising antibody response from 9 dpi, and no major abnormalities in leukocyte numbers. Faecal shedding lasted for 28-56 days, but virus shed during this stage was less infectious in enterocyte cultures and affected by mutations. Remarkably, in the other cat neither clinical signs nor acute shedding were seen, but virus was detected in blood cells from 3 dpi, and shedding of non-enterotropic, mutated viruses suddenly occurred from 14 dpi onwards. Neutralising antibodies arose from 21 dpi. Leukocyte numbers were not different compared to the other cats, except for the CD8 + regulatory T cells. These data indicate that FECV can infect immune cells even in the absence of intestinal replication and raise the hypothesis that the gradual adaptation to these cells can allow non-enterotropic mutants to arise. Feline coronaviruses (FCoVs) occur as two pathotypes, associated with either enteric or systemic diseases in cats. Feline enteric coronavirus (FECV) is an enterotropic virus, ubiquitously present in the cat population 1,2 . The enteritis caused by the intestinal replication can manifest as a transient anorexia, weight loss and/or diarrhoea, but clinical signs are often too mild to be noticed 1,3,4 . Feline infectious peritonitis virus (FIPV) most likely arises from FECV by accumulation of mutations in individually infected cats [5] [6] [7] [8] [9] [10] [11] . These yet not fully characterized mutations abrogate the enterocyte tropism but provide the virus with tools to productively replicate in monocytes/macrophages, causing a highly fatal systemic disease, feline infectious peritonitis (FIP), which is characterised by a diffuse vasculitis, polyserositis and severe lymphopaenia 12-17 . To date, it remains unknown where, when, and how this pathotype switch is induced in FECV-infected cats. Due to its pathogenic behaviour, FIPV has received considerable attention, and clinical, virological, and immunological parameters during both natural and experimental FIPV infections have frequently been studied 14-16 . The last decade, comprehensive studies on the FIPV parent virus, FECV, have extensively contributed to our current understanding of the epizootiology and pathogenesis 4,18-20 , but many crucial virological and immunological data on the FECV-cat interactions are missing to fully understand the behaviour of this FIPV parent virus. Due to the lack of an FECV-susceptible cell line, there is so far no information on the infectivity (and its
A:
Experimental feline enteric coronavirus infection reveals an aberrant infection pattern and shedding of mutants with impaired infectivity in enterocyte cultures OPEN