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.

Zika virus (ZIKV) infection can be the cause of congenital malformations, including microcephaly in infants and can cause other disorders such as Guillain-Barré syndrome, meningoencephalitis, and myelitis, which can also occur in some infected adults. However, at this time, there is no drug approved to treat ZIKV infection. Drug repurposing is the promptest way to obtain an effective drug during a global public health emergency such as the spread of Zika virus. In this study, we report a US Food and Drug Admistration-approved drug that is safe for pediatric use. Nitazoxanide and its bioactive metabolite, tizoxanide, have anti-ZIKV potential in vitro, and we identified that they exerts antiviral effect possibly by targeting the viral postattachment step.
Pediatric Drug Nitazoxanide: A Potential Choice for Control of Zika

Newcastle disease (ND) is a contagious disease that affects most species of birds. Its causative pathogen, Newcastle disease virus (NDV), also exhibits considerable oncolytic activity against mammalian cancers. A better understanding of the pathogenesis of NDV will help us design efficient vaccines and novel anticancer strategies. GW3965, a widely used synthetic ligand of liver X receptor (LXR), induces the expression of LXRs and its downstream genes, including ATP-binding cassette transporter A1 (ABCA1). ABCA1 regulates cellular cholesterol homeostasis. Here, we found that GW3965 inhibited NDV infection in DF-1 cells. It also inhibited NF-jB activation and reduced the upregulation of proinflammatory cytokines induced by the infection. Further studies showed that GW3965 exerted its inhibitory effects on virus entry and replication. NDV infection increased the mRNA levels of several lipogenic genes but decreased the ABCA1 mRNA level. Overexpression of ABCA1 inhibited NDV infection and reduced the cholesterol content in DF-1 cells, but when the cholesterol was replenished, NDV infection was restored. GW3965 treatment prevented cholesterol accumulation in the perinuclear area of the infected cells. In summary, our studies suggest that GW3965 inhibits NDV infection, probably by affecting cholesterol homeostasis.
The LXR ligand GW3965 inhibits Newcastle disease virus infection by affecting cholesterol homeostasis

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

Experimental feline enteric coronavirus infection reveals an aberrant infection pattern and shedding of mutants with impaired infectivity in enterocyte cultures OPEN