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Experimental Infection of Domestic Cats with Feline Herpesvirus-1 Strain CH-B Isolated from British Shorthair Cat

病毒 病毒学 结膜 发病机制 医学 呼吸道 病毒潜伏期 上呼吸道感染 牛疱疹病毒1型 生物 疱疹病毒科 免疫学 呼吸系统 病毒复制 病毒性疾病 内科学
作者
Jiangting Niu,Han Zhao,Shuang Zhang,Yanbing Guo,Qian Zhang,Di Bao,Hao Dong,Fanxing Meng,Yanli Zhao,Hailong Huang,Junzheng Wang,Kai Wang,Guixue Hu,Shushuai Yi
出处
期刊:Research Square - Research Square
标识
DOI:10.21203/rs.3.rs-94561/v1
摘要

Abstract Background: Feline herpesvirus-1 (FHV-1) is a most common virus that cause viral rhinotracheitis and ocular diseases in domestic cats and wild felids. As other alpha-herpesviruses, acute FHV-1 infection is responsible for severe upper respiratory tract and ocular disease, followed by lifelong latency that persist the limited virus in sensory neuronal cells. While latency reactivation can result in recrudescence, leading sever ocular lesions. Hence, FHV-1 infection in cats can be considered as a good natural host model to study alpha-herpesvirus pathogenesis. Results: In this study, the FHV-1 CH-B was isolated from nasal discharge collected from a British shorthair cat in China, and was further identified via transmission electron microscopy (TEM) observation, indirect immunofluorescence assay (IFA) and genome analysis. Experimental infection of domestic cats with different dose of isolate CH-B, ranging from 10 4 to 10 7 TCID 50 , showed that cats inoculated with 10 5 TCID 50 not only showed typical upper respiratory track and ocular symptoms, but also could copy the progress of disease development. Therefore, the FHV-1 infection model was established by intranasally inoculated with 10 5 TCID 50 of FHV-1 isolate CH-B. Infected cats began to show clinical signs at days 5 post inoculated (dpi), developed severe upper respiratory tract and ocular symptoms at 10-15 dpi, began to recover at 20 dpi, and recovered almost completely by 25 dpi. During acute infection period, virus mainly replicates in turbinate, conjunctiva, cornea and sensory neuronal cells, while virus only persists in trigeminal ganglia (TG) at lifelong latency. Viremia and viral infections in lungs do not appear in FHV-1 CH-B infected cats, with only one exception. We also demonstrate that FHV-1 CH-B infection can induce severe inflammatory responses and lung, trachea, and tonsils tissues damage in cats. In addition, we found that FHV-1 infected cats can shed virus via nasal and ocular discharge, resulting FHV-1 infection in in-contact cats. Conclusions : This natural host model of FHV-1 infection will be valuable for the screen and assessment of antiviral drugs and vaccines, as well as the studies of the pathogenesis of alpha-herpesvirus infection in animals and humans.

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