Rhinovirus

• 4.1 Routes of infection
• 4.2 incubation
• 4.3 Infection Symptoms
• 4.4 Treatment and prevention
• 4.5 Environmental stability

Construction

Virion

Due to the homology rhinoviruses are divided into three species (A to C). Rhinoviruses are non-enveloped, which means they do not have lipid layer as a shell. Their diameter is between 24 nm and 30 nm, and thus they are more likely to be small viruses (150 S in a density gradient ). They are compared with the closely related enteroviruses relatively sensitive to acid and is therefore not resistant to gastric juices, but heat-stable and have a narrow host tropism, and replication closer conditions ( lower temperatures and not in the intestinal tissue). Each capsid protein occurs 60 times before in the icosahedral capsid of the virion with cubic symmetrical structure. In the middle of each of the 20 faces of the capsid is a depression ( engl. canyon, gorge ') for binding of the receptor. The capsid has a layer thickness of about 5 nm Approximately 90 % of the strains of species A and B use ICAM -1 as a cellular receptor, and the remaining ten percent use the LDL receptor. The strains of the species C. used a previously unknown cellular receptor.

Genome

Rhinoviruses are RNA viruses with a single stranded RNA genome of positive polarity of approximately 7.2 to 8.5 kilobases in length. The viral proteins are produced as a polyprotein of about 2200 amino acids, followed by two ( by the two pro- 2Apro and 3Cpro genes coded ) proteases into the individual proteins cleaved. Located in the virion structural proteins are encoded in the 5'- region of the RNA, the non-structural proteins in the 3 'region (as with all picornaviruses ). At the 5 ' end is a 5' UTR followed by the regions P1 (Gene 1A -D of the four capsid proteins VP1 -4), P2 ( 2Apro genes, 2B, 2C), P3 (3A, 3B, 3Cpro, for 3Dpol the VPg, protease and RNA polymerase), the 3 ' UTR (redundant in a cell culture ), and a poly -A tail. The 5'-end of the viral RNA associated with the viral protein VPg.

Proteins

Rhinoviruses have all as picornaviruses four capsid proteins ( VP1 to VP4 ), the partially used in addition to the packaging of the genome as a receptor for attachment to a cell. The VP4 connects the outer to the virion proteins VP1, VP2 and VP3 with the genome. VP1 -3 are identified as surface proteins amplified by antibodies. Upon binding of the cellular receptor of the N -terminus of the VP1 is swept out of the virion to the outside and release the VP4, which together form a pore of penetrating the cell membrane, by which the viral RNA is funneled into the cytosol. 2Apro protein is a cysteine ​​protease cleavage of the polyprotein from the P1 and P2 region. Protein 2B serves to destabilize the cell membrane to facilitate the release of newly formed virions from the cell. 2C protein has a previously unknown function. 3A protein is a membrane protein for binding of the newly formed virions at the cell membrane to facilitate the release. Protein 3B ( syn. VPg ) binds to the 5'-end of the viral RNA and has been unknown other functions. 3Cpro protein is a cysteine ​​protease that cleaves the cellular proteins Nup153, Nup214 and Nup358, thereby interrupting the discharge of molecules from the cell nucleus. 3DPol protein is an RNA polymerase to amplify the viral RNA. The proteins VP1 and VPg 4 occur in the virion and are therefore called structural proteins.

Replication cycle

By binding to the respective receptor occurs a penetration of the cell membrane by the pore-forming proteins VP1 and VP4, where the viral RNA to the ribosome the viral polyprotein is produced. Replication of the viral RNA is done according to a smooth transfer to the endoplasmic reticulum by the RNA polymerase 3DPol. The copied genomes are funneled from the endoplasmic reticulum into the cytosol, where together the viral RNA with the viral proteins into virions. Rhinoviruses are lytic viruses, and leave the host cell by destroying precisely this.

Occurrence

Rhinoviruses but are spread throughout the world and limited to humans, prefer temperatures of 3 ° C to 33 ° C, they also absolutely need in order to replicate. At higher temperatures - for example, at body temperature (36 ° C to 37.5 ° C), however, their growth is inhibited. This preference for cooler temperatures caused the higher infection rate in cold, wet weather and the tropism for the cooler nasal mucosa. Since the blood vessels contract when it has cooled bodies in the nasal mucosa, the temperature of the nasal mucosa falls into the range that is optimal for these viruses.

Infection

Routes of infection

Rarely is the infection caused by the transmission of viruses in droplets of different body fluids that are ejected when sneezing or coughing of an infected person and then be transferred to another person by droplet infection instead. Far more often is the direct transmission, eg via contaminated hands or indirectly via objects ( smear ). Infected are particularly often people whose weakened immune system, or - are not trained properly - as in babies and young children.

Incubation period

The incubation time is relatively short. After one to four days, viruses are detectable in the nose, followed by two to three days viruses are produced until the adaptive immune response is engaged. After about 12 hours the first finished viruses leave the host cell and infect the next.

Infection symptoms

Rhinoviruses infect the mucous membranes of the nose and throat, remain strictly localized and do not cause generalized infection. The result is a runny nose - less common in children with bronchitis. The human body responds to the virus attacks with an inflammatory response of the nasal mucosa. The vessels of the mucous membrane become more permeable, liquid comes out, the nose runs. Later, the nasal mucosa swells, up to a half inch thickness, making breathing through the nose is as good as impossible. In addition, malaise and headache policy. Frequently occurs in addition to the viral infection or secondary infection by bacteria in the throat and pharynx on.

Treatment and prevention

A combat viruses, it is hardly possible, but not necessary, because the human immune system alone with these viruses is done. It takes about a week until our body has adjusted to the viral attacker, therefore, a cold is by this time mostly over. The rhinoviruses addressed in the nasal mucosa in the long run do no harm. In general, however, the symptoms are treated with medication to make it easier to survive the disease.

In the 1960s, several vaccines have been generated, however, could only produce a strain-specific vaccine protection. A rhinovirus infection leads to the formation of neutralizing antibodies, but produces only one strain-specific immunity. Rhinoviruses RNA viruses tend to be in the course of the immune evasion to increased mutation and the capsid proteins of four typical rhinovirus strains are only between 41% to 83 % identical to each other, which complicates the formation of a stem cross- immunity. In people who have had multiple infections of different strains, the disease duration is slightly shortened.

Prevention is by exposure prophylaxis (eg, avoidance of crowds and hand washing ) is possible, since one can not establish long-term effective drugs or vaccines due to the large number of serotypes and the only type-specific immunity. In addition, the antiviral drug pleconaril prevents the unpacking of the viral genome is not resistant rhinoviruses.

Environmental stability

Rhinoviruses have picornaviruses as compared to other viruses have a relatively high tenacity, but they are in contrast to the related acid-sensitive enterovirus. The Tenacity of rhinoviruses includes due to the lack of viral envelope has a relatively high resistance to alcohols ( eg, ethanol, isopropanol) and surfactants, but they can be largely removed by hand washing of the hands. Rhinoviruses are sensitive to acids, alkylating agents, and physical disinfection methods.