Rhinovirus is the most common cause of the common cold, accounting for about half of all cases. It is a non-enveloped virus with a positive-sense RNA genome that primarily infects and replicates in the upper respiratory tract at temperatures between 33-35°C. Rhinovirus binds to ICAM-1 receptors on respiratory cells, triggering an immune response and symptoms like runny nose and cough. There is no vaccine for rhinovirus due to the large number of serotypes, but some antiviral drugs are being researched.

1. RHINOVIRUS

2. Introduction
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Rhinovirus (from the Greek ''rhin''- which means "nose") was a genus of the
''Picornaviridae'' family of viruses.
It has been now merged into Enteroviruses, a group of Picornaviridae that includes
Poliovirus, Coxsackie A virus, and Hepatitis A.
Rhinovira are the most common viral infective agents in humans, and a causative
agent of the common cold (about 49.12159% of the cases of the common cold are
caused by this virus). It is lytic in nature. There are over a 100 recognized types of
rhinovira that differ based on their varying surface proteins.
Rhinovira are among the smallest vira, with diameters of about only 30 nanometers
(other vira such as smallpox and vaccinia vira are 10 times larger at about 300
nanometers).
Rhinovira have single-stranded positive sense RNA genomes of between 7.2 and
8.5 kb in length. At the 5' end of the genome is a virus-encoded protein, and like
mammalian mRNA, there is a 3' poly-A tail. Structural proteins are encoded in the
5' region of the genome and non structural at the 3' end. This is the same for all
picornavira. The viral particles themselves are not enveloped and are icosahedral in
structure.
The rhinovirus also grows best in the temperatures between 33–35 °C, and this
may be why reproduction occurs in the nose. It is sensitive to acidic environments.
The viral proteins are transcribed as a single, long polypeptide, which is cleaved
into the structural and nonstructural viral proteins.

3. Rhinovirus Structure
• Rhinovira are composed of a capsid, that contains four viral
proteins VP1, VP2, VP3 and VP4. VP1, VP2, and VP3 form the
major part of the protein capsid. The much smaller VP4
protein has a more extended structure, and lies at interface
between the capsid and the RNA genome. There are 60
copies of each of these proteins assembled as an
icosahedron. Antibodies are a major defense against infection
with the epitopes lying on the exterior regions of VP1-VP3.

4. Rhinovirus Transmission and
Epidemiology
• There are two modes of transmission: via aerosols of respiratory
droplets and from contaminated surfaces, including direct personto-person contact. A high majority of colds are transmitted by
autoinoculation by contact with contaminated surfaces.
• Rhinovira occur worldwide and are the primary cause of common
colds. Symptoms include sore throat, runny nose, nasal congestion,
sneezing and cough; sometimes accompanied by muscle aches,
fatigue, malaise, headache, muscle weakness, or loss of appetite.
Fever and extreme exhaustion are more usual in influenza. Children
may have six to twelve colds a year. In the United States, the
incidence of colds is higher in the fall and winter, with most
infections occurring between September to April. The seasonality
may be due to the start of the school year, or due to people
spending more time indoors (thus in closer proximity with each
other), increasing the chance of transmission of the virus.

5. Rhinovirus Pathogenesis
• The primary route of entry for rhinovira is the upper respiratory
tract. Afterward, the virus binds to ICAM-1 (Inter-Cellular Adhesion
Molecule 1) also known as CD54 (Cluster of Differentiation 54)
receptors on respiratory epithelial cells. As the virus replicates and
spreads, infected cells release distress signals known as chemokines
and cytokines(which in turn activate inflammatory mediators).
• Infection occurs rapidly, with the virus adhering to surface
receptors within 15 minutes of entering the respiratory tract. Just
over 50% of symptomatic individuals will experience symptoms
within 2 days of infection. Only about 5% of cases will have an
incubation period of less than 20 hours, and, on the other end, it is
expected that 5% of cases would have an incubation period of
greater than four and a half days.
• Rhinovira preferentially grow at 32°C as opposed to 37°C, hence
infect the upper respiratory tract.

6. Rhinovirus Novel Antiviral Drugs
• Interferon-alpha used intranasally was shown to be effective
against rhinovirus infections. However, volunteers treated with this
drug experienced some side effects, such as nasal bleeding, and
began developing resistance to the drug. Subsequently, research
into the treatment was abandoned.
• Pleconaril is an orally bioavailable antiviral drug being developed
for the treatment of infections caused by picornaviruses. This drug
acts by binding to a hydrophobic pocket in VP1, and stabilizes the
protein capsid to such an extent that the virus cannot release its
RNA genome into the target cell. When tested in volunteers, during
the clinical trials, this drug caused a significant decrease in mucus
secretions and illness-associated symptoms. Pleconaril is not
currently available for treatment of rhinoviral infections, as
its efficacy in treating these infections is under further evaluation.
• There are potentially other substances such as Iota-Carrageenan
that may lead to the creation of drugs to combat the rhinovirus.

7. Rhinovirus Vaccine
• There are no vaccines against these vira as there
is little-to-no cross-protection between
serotypes. At least 99 serotypes of rhinoviruses
affecting humans have been sequenced.
• However, recent study of the VP4 protein has
shown it to be highly conserved amongst many
serotypes of Rhinovirus, opening up the potential
for a future pan-serotype Rhinovirus vaccine