Clinical Microbiology: Open Access

Aspects of Enteroviruses Accelerates Autoimmunity in Type 1 Diabetes

Fatima Talib^* Department of Microbiology, Jazan University, Jazan, Saudi Arabia
^*Correspondence: Fatima Talib, Department of Microbiology, Jazan University, Jazan, Saudi Arabia, Email:

Received: 31-Mar-2023, Manuscript No. CMO-23-21317; Editor assigned: 03-Apr-2023, Pre QC No. CMO-23-21317(PQ); Reviewed: 17-Apr-2023, QC No. CMO-23-21317; Revised: 24-Apr-2023, Manuscript No. CMO-23-21317(R); Published: 02-May-2023, DOI: 10.35248/2327-5073.23.12.337

Description

Enteroviruses (EVs) are non-enveloped, small, single-stranded and positive-sense RNA viruses belonging to Picornaviridae family. The Enterovirus genus has 15 species, 7 of which infect humans (enteroviruses A to D and rhinoviruses A to C), and over 250 serologically distinct viruses. There are over 110 serotypes of enteroviruses A-D, the best known of which are poliovirus, enterovirus A71, echovirus, coxsackievirus A, and coxsackievirus B (CVB). These viruses are ubiquitous worldwide and are seasonally transmitted primarily through oral or respiratory patterns. EV infection is common in summer and early autumn in temperate zones, but constant throughout the year in the tropics.

They grow primarily in the gastrointestinal or upper respiratory tract and can spread to various target organs via the lymphatic system and bloodstream. Although they are cytolytic viruses, they can cause persistent infections both in vitro and in vivo. Most enteroviral infections remain asymptomatic but cause numerous clinical signs of varying severity, depending on the site of infection and viral serotype. Enteroviral infections range from relatively mild symptoms such as colds, fevers, and skin lesions to severe symptoms such as meningitis, hepatitis, encephalitis, myocarditis, pancreatitis, hand-foot-and-mouth disease, pericarditis, neonatal sepsis, and acute flaccid paralysis can cause acute symptoms of In addition to acute illnesses, electric vehicles have also been linked to chronic illnesses such as his type-1 diabetes.

The electric vehicle genome contains a single open reading frame of approximately 7400 bases flanked by untranslated regions at the 5' and 3' ends. The CVB replication cycle consists of various steps. Briefly, virus particles bind to specific cell surface receptors, mainly Coxsackie and Adenovirus Receptors (CAR) and co-receptors. B. Damping acceleration factor. Depending on the serotype and cell type, virus-cell receptor interactions result in the internalization of the virus through different endocytic pathways. After viral internalization, receptor binding and low endosomal pH induce a conformational change in the viral capsid, resulting in release of the viral genome through the endosomal membrane into the cytoplasm. Translocation of the viral RNA the cytoplasm through membrane channels was described in poliovirus that cannot be ruled in CVB. Viral proteins involved in viral replication are potential targets for antiviral drugs.

Pleconaril is one of the most studied antiviral drugs, originally developed to treat the common cold and to prevent asthma exacerbations caused by picornavirus infection. Pleconaril binds to the viral capsid, inhibits its attachment and uncoating to cellular receptors, and prevents the release of viral RNA. It was rejected by the US Food and Drug Administration (FAD) due to the emergence of resistant virus. In vitro and in vivo antiviral activity of pleconaril against some electric vehicles such as CVB3 has been reported. Ribavirin is a nucleoside analogue which was approved by FDA as antiviral agent for the treatment of chronic hepatitis-C virus infection in combination of peginterferon. Ribavirin can affect viral replication by inducing lethal mutagenesis through interaction with viral proteins.

Some drugs, such as fluoxetine, which targets the nonstructural viral 2C protein, the antifungal drug itraconazole, which targets the nonstructural viral protein, and the antiprotozoan emetine, which inhibits IRES activity, have anti-CVB activity. There is increasing interest in researching the antiviral activity of repurposed drugs as they may progress rapidly into clinical trials. Fluoxetine can inhibit replication of pancreatic cells in vitro in models of acute and persistent infection and in infected human organs in vivo. Pleconaril and Hizentra, human immunoglobulin concentrates containing anti-EV-neutralizing IgG antibodies, may also inhibit persistent infection of pancreatic cells. However, the emergence of fluoxetine-resistant variants has been observed during treatment of persistently infected pancreatic cell cultures.

Enviroxime kinase inhibitor inhibits CVB replication by targeting the host factor phosphatidylinositol 4-kinase type IIIβ which involved in the plus-strand RNA synthesis. Enviroxime can also inhibit persistent infection of pancreatic cells. Itraconazole can also interfere with RNA replication by targeting cellular Oxysterol-Binding Proteins (OSBPs) involved in cholesterol and Phosphatidylinositol-4-Phosphate (PI4P) transport and cell signaling.