Recombinant Human Rhinovirus 16 VP2 (a.a. 70-330) [His]

Human rhinovirus (HRV) was first discovered in the 1950s. Since Price isolated the first strain using tissue culture methods, more than 120 HRV serotypes have been identified. It is the virus with the most serotypes in humans, along with influenza viruses. Influenza viruses and respiratory syncytial virus are considered to be the major causes of respiratory tract infections.

Figure 1. Cryoelectron microscopy of human rhinovirus (HRV)-16 particles and their complex with D1D2. (Sources: Olson NH, et al.1993)

HRV belongs to the genus Enterovirus of the family Picornaviridae. It is a single-stranded positive-strand RNA virus with a genome of approximately 7200 bp, a single open reading frame and a 5' non-coding region consisting of a short peptide. Its structure is a 20-27 nm diameter, non-enveloped 20-sided virion. The 4 protein subunits VP1, VP2, VP3 and VP4 form a protein capsid with 60 capsomers. The remaining non-structural proteins participate in viral genome replication and assembly. VP1, VP2 and VP3 proteins express the antigenic diversity of the virus, while VP4 fixes the viral RNA core to the capsid internally. Each of these four capsid proteins has 60 protein protrusions, giving the virion an icosahedral structure. There is a canyon in VP1, which is the site for HRV to bind to host cell surface receptors. Depending on the type of receptor, viral replication is taken up by endocytosis or pinocytosis. Among the known HRV serotypes, more than 90% use the cell surface receptor intercellular adhesion molecule-1 (ICAM-1) to enter cells, and a few enter cells through low-density lipoprotein receptor (LDLR) attachment. Some antiviral drugs can induce canyon changes, inhibiting viral adhesion and viral uncoating. Due to the lack of a lipid envelope, HRV is inactivated in organic solvents such as ether, chloroform, ethanol and 5% benzene. HRV is heat-sensitive and loses infectivity at 50°C to 56°C. HRV is the virus with the most human serotypes, including HRVlA, HRV1B, HRV2-HRV86 and HRV88-HRVl00. HRV87 is currently identified as a nucleic acid-sensitive strain of enterovirus 68. Some cross-neutralization tests have shown that HRV has no group antigens. According to phylogenetic sequence standards, HRV is divided into three species: HRV-A, HRV-B and HRV-C. Currently, 77 serotypes of HRV-A, 25 serotypes of HRV-B, and 51 serotypes of HRV-C have been found. HRV-C is the newest and most unique of all human rhinovirus species. Studies on HRV-C have shown that this species uses a unique cell attachment mechanism. Human Rhinovirus 16 VP2 is the protein subunit VP2 of HRV16 serotype.

Human RV(rhinovirus) infection begins with the binding and translocation of nonenveloped virions to cells. The genetic material is then released into the cytoplasm, where host ribosomes convert the positive single-stranded RNA into a polyprotein, which is cleaved to form 11 new viral proteins that eventually mature into a new virus particle. RV-infected cells induce monocytes to upregulate the expression of viral receptors, facilitating the spread of the virus to other cell types. RV is the most common virus causing respiratory disease in children. Its disease burden ranges from mild common colds and acute otitis media (AOM) to severe wheezing. Although RV usually causes acute infection, RV has also been reported to be associated with chronic respiratory diseases, immune system diseases, and chronic obstructive pulmonary disease. Asthmatic diseases (bronchiolitis, recurrent wheezing, or asthma exacerbations) are often associated with RV (11, 12, 23, 26-28), and RV-induced wheezing in infancy may be the first symptom of childhood asthma. Studies have shown that RV infection can lead to an increased risk of asthma, with an approximately 5-fold risk of asthma after respiratory syncytial virus-induced wheezing, but a 10-fold risk of asthma after RV-induced wheezing. RV, as the main trigger of acute asthma exacerbation, can not only infect bronchial epithelial cells and induce the production of proinflammatory factors, but also induce angiogenesis and the production of proinflammatory mediators. A large amount of evidence shows that there is a link between early RV infection and asthma attacks and exacerbations, but RV-induced wheezing is only an important risk factor for asthma when atopic asthma occurs. Many evidences support that sensitization is a risk factor for RV-induced early wheezing, which in turn is a risk factor for asthma. In additon, RV is one of the most common causes of lower respiratory tract infections in children and is often found in community-acquired pneumonia (CAP). RV is the main non-RSV pathogen that causes hospitalization of children with bronchiolitis and pneumonia. RV is also one of the common pathogens that cause pertussis-like syndrome. The role of RV as a true pneumonia pathogen is unclear and may be related to the original lower respiratory tract disease in children. RV is also a pathogen of severe exacerbation of chronic obstructive pulmonary disease. In addition to causing respiratory diseases, RV can also cause some neurological diseases.

Capsid Protein VP2
HRV-16 VP2
Rhinovirus VP2
VP2 Protein
VP2 Structural Protein
Human Rhinovirus VP2
HRV VP2