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Cardiovirus is a genus of viruses in the order Picornavirales, in the family Picornaviridae. Human's and vertebrates serve as natural hosts for this virus that causes enteric infections. There are currently three species in this genus including the type species Cardiovirus A, Cardiovirus B, and Cardiovirus C. Diseases associated with this genus include: myocarditis, encephalitis, multiple sclerosis, and type 1 diabetes.

Cardiovirus A is composed of only one serotype, encephalomycarditis virus (EMCV). While Cardiovirus B consists of four viruses which are probably serologically distinct; these are Theiler's Murine encephalomyelitis virus (TMEV), Vilyuisk human encephalomyelitis virus (VHEV), a Theiler-like rat virus (TRV) (which has yet to be named) and Saffold virus (SAF-V). Of these 4 viruses of Cardiovirus B predominately only VHEV and SAF-V are seen to cause infection in humans. Thus far Cardiovirus C has only been observed in brown rats, and is novel.

Viruses in Cardiovirus are single-stranded RNA non-enveloped, with icosahedral, Spherical, and Round geometries, and T=pseudo3 symmetry. The diameter is around 30 nm. Genomes are linear and non-segmented, around 7.8kb in length. Due to the icosahedral nature of Cadiovirus it is able to contain 60 protomers, each of these contain the 4 polypeptides VP1, VP2, VP3, and VP4. Inside isocohedral capsid of this virus there is a positive single-stranded RNA, and is composed of untranslated regions on both the 3' and 5' ends of the genome. These untranslated regions of genome are important for the replication of the virus, with the untranslated region on the 5' side being the location of internal ribosomal entry site (IRES). The IRES important in leading the translation of the genome.

Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the virus to host receptors, which mediates endocytosis. Replication follows the positive stranded RNA virus replication model. Positive stranded rna virus transcription is the method of transcription. Translation takes place by -1 ribosomal frameshifting, viral initiation, and ribosomal skipping. The virus exits the host cell by lysis, and viroporins. Human and vertebrates serve as the natural host. Transmission routes are zoonosis and fomite.

The 3’ end of the genome encodes a polyA tail while the 5’ end encodes a genome-linked protein. A unique feature of this genus is the presence of the L* protein, 18kDa, that is made out of frame from the polyprotein and is present in the DA subgroup of TMEV. It has been found to be important for the virus pathogenesis.

In the case of Cardiovirus A, the virus can cause encephalitis and myocarditis, mostly in rodents, which are natural hosts. The virus is transmitted from rodents to other animals. Severe epidemics have been seen in swine and elephants.

Replication of cardioviruses is dependent on a structured RNA element called the Cardiovirus cis-acting replication element (CRE).

Human cardioviruses were first isolated in 1981. Seven additional isolates have since been described. They have been associated with gastroenteritis, influenza-like symptoms and non- polio-associated acute flaccid paralysis in North America, Europe and South Asia.

The first infection of cardiovirus in humans was identified in the stool sample of an infant that was experiencing fever of unknown origins in 2007. It was subsequently named the Saffold virus after the lead researcher, Morris Saffold Jones.

Other pathogenic cardioviruses isolated from humans include the Syr-Darya valley fever virus and Vilyuisk human encephalomyelitis virus.