HERPESVÍRUS FELINO 1: MECANISMOS CELULARES DA INTERAÇÃO HOSPEDEIRO-VÍRUS
HERPESVÍRUS FELINO 1: MECANISMOS CELULARES DA INTERAÇÃO HOSPEDEIRO-VÍRUS
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DOI: https://doi.org/10.22533/at.ed.81924090410
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Palavras-chave: Herpesvírus Felino 1; microRNAs; Autofagia; Endocitose; Estratégias terapêuticas.
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Keywords: Feline Herpesvirus 1; microRNAs; Autophagy; Endocytosis; Therapeutic strategies.
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Abstract: Feline herpesvirus type 1 (FHV-1) is an enveloped DNA virus belonging to the Herpesviridae family, being one of the most prevalent in cats, causing feline viral rhinotracheitis, responsible for more than half of viral diseases of the upper respiratory tract and can lead to eyes lesions resulting in loss of vision. Although the course of the disease is mostly mild, FHV-1 infections can also cause severe symptoms, including pneumonia, gastritis, and necrotizing bronchiolitis. Meanwhile the available vaccine reduces the severity of the disease, it does not prevent infection or limit the spread of the virus. Interestingly, FHV-1 uses different replication and internalization pathways depending on the cell type and tissue, which constitute important regulatory factors in the host and participate in the pro- or antiviral role. In this chapter, we will address 3 different pathways: 1) receptor- mediated endocytosis, a process in which FHV-1 generally uses heparan sulfate proteoglycans (via glycoprotein B) to bind to the susceptible cell, and glycoprotein C that allows or enhances the interaction of the virus with the receptor, while glycoprotein D mediates endocytosis by interacting with the entry receptor. Internalization can occur by pH-dependent endocytosis mediated by dynamin or caveolin. 2) microRNAs (miRNAs), which are involved in regulating FHV-1 replication in the host through direct targeting of the viral genome and indirect targeting of host genes to modulate the virus life cycle. In general, viral infection can alter the host's miRNA expression profile and even develop its own miRNA systems to maintain an environment conducive to infection, proliferation or latency. On the other hand, the host also upregulates the expression of cellular miRNAs with antiviral function to inhibit virus replication. 3) Autophagic process, in which some inhibitors have been described, which block the fusion of autophagosomes with lysosomes, reducing the proliferation and viability of FHV-1. Elucidating the mechanisms of FHV-1 entry may support future efforts to limit virus transmission or develop new antivirals.
- Ana Carolina Guimarães Faleiros
- Vitória Baruc Santos MENEZES;
- Nicole CANABARRO,
- Eduardo Fernandez de SANTANA;
- Emerson Ticona FIORETTO.
