Recombinant Human Rhinovirus 16 VP1 (a.a. 565-853) [His]

Most prevalent acute respiratory disease among children is caused by Human Rhinovirus (HRV). HRV usually appears in the runny nose, cough, and sore throat you get with a cold. But the most recent findings show that HRV isn't only linked to upper respiratory infection – it can lead to lower respiratory infection, increased asthma and other grave complication. HRV can sometimes be conflated with bacterial infection and thus present as more of a clinical puzzle. The HRV diagnosis is as high as 50% for acute otitis media, for instance. HRV can also lead to dysfunction of the bronchi that can add to the asthmatic's condition.

HRV is an envelopeless virus in the genus Picornaviridae. It is icosahedral, with a single-stranded positive-sense RNA genome. There are 11 proteins encoded in an open reading frame in HRV genome; the four main structural proteins are VP1, VP2, VP3, and VP4. They fuse the virus capid. VP1, VP2 and VP3 compose the main structure of the capsid, and are the engine of the virus's antigenic diversity as well as its binding to host cell receptors. VP4 is housed in the capsid and it helps to hold the RNA genome together. HRV is divided into A, B and C genetic types (the latest identified type is HRV-C). HRV-C particularly is linked to asthma in children because infections can worsen asthma and other chronic lung disorders.

Figure 1. Human rhinovirus genomic organization, virion structure, and species
(Source: Stobart CC, et al. 2017)

HRV travels into host cells via intercellular adhesion molecule-1 (ICAM-1) present on their surface; some subtypes even reach the cells via low-density lipoprotein receptors (LDLR). When infected, the virus is absorbed through endocytosis or pinocytosis, where it releases its RNA genome and starts replication. Most studies confirm that HRV infection leads to an increased release of various cytokines, resulting in impaired barrier function of the airway epithelium, along with inflammation, repair, and remodeling of the airways. Furthermore, HRV does not cause significant cell necrosis during host infection; instead, immune damage is considered its primary pathogenic mechanism. Interferons (IFNs) play a crucial role in the non-specific defense mechanisms against viral infections and in regulating immune responses, with IFN1 and IFN3 being significant interferons secreted by airway epithelial cells during RV infection.

Recombinant HRV 16 VP1