Morphology and genome structure
Rotaviruses are spherical in shape with a diameter of 80 nm. The genome is represented by fragmented double-stranded RNA (dsRNA), which consists of 11 segments. Each RNA molecule includes both plus- and minus-strands.
Virions lack an outer envelope, but possess a unique triple-layered capsid consisting of 12 proteins. Visually, it resembles a wheel:
- Inner capsid is formed by the VP-2 protein.
- Intermediate capsid ("spokes") consists of the VP-6 protein.
- Outer capsid is formed by the type-specific VP-7 antigen and spikes made of the VP-4 protein (hemagglutinin and attachment protein).
Viral life cycle
Rotavirus replication is a complex process that begins with the cleavage of the VP-4 protein by gastrointestinal tract enzymes into VP-5 and VP-8 subunits. This is necessary for virion activation.
- Penetration: The VP-8 subunit binds to sialic acids of the target cell, after which the virus enters via endocytosis.
- Transcription: Inside the endosome, the virion loses its outer layer, turning into a double-layered particle. In the cytosol, the polymerase complex (VP-1 and VP-3) is activated, synthesizing (+)RNA.
- Protein synthesis and assembly: Non-structural proteins (NSP-2 – NSP-5) form viroplasms — the sites for assembly of new particles and genome replication.
- Maturation: Double-layered particles move to the endoplasmic reticulum (ER), where the outer capsid is assembled with the help of the NSP-4 protein.
- Release: New virions leave the cell either by lysis or via exocytosis.
Pathogenesis and epidemiology
Non-structural viral proteins play an important role in the development of the disease. Of particular significance is NSP-4, the first described viral enterotoxin. It is responsible for the development of secretory diarrhea.
Rotaviruses are divided into 7 serogroups (A–G). Serogroups A, B, and C cause disease in both humans and animals, whereas the rest are pathogenic only to animals. The causative agent exhibits high persistence in the environment. Transmission occurs via the fecal-oral mechanism (primarily waterborne, as well as through food and household items).
Briefly: answers to topical questions
What clinical symptoms are characteristic of rotavirus infection in children?
Rotavirus infection in children is characterized by an acute onset with gastroenteritis, fever, and catarrhal syndrome. Full manifestation of symptoms develops within the first 24 hours.
Main clinical manifestations:
- Gastroenteritis — includes vomiting, abdominal pain, and frequent watery diarrhea (secretory diarrhea with a frequency of 10–15 times per day).
- Fever — body temperature rises to 38.5 °C and above.
- Catarrhal syndrome — often precedes diarrhea, causing combined lesions of the respiratory system and gastrointestinal tract in 60–70% of patients.
The duration of acute manifestations of the disease is usually 1–2 days.
To remember the capsid structure, use the "wheel" rule: Inside is the axle (VP-2), from it extend the spokes (VP-6), and on the outside is the tire (VP-7) with spikes for road grip (VP-4).
Class and exam questions
Which protein is responsible for virus adsorption?
The outer capsid protein VP-4 (specifically its VP-8 subunit) is responsible for attachment to the cell.
Where does the assembly of new viral particles take place?
Intracellular assembly and genome replication take place in special cytoplasmic inclusions called viroplasms.
Why does the virus cause diarrhea?
Rotavirus synthesizes the non-structural protein NSP-4, which acts as a viral enterotoxin and stimulates secretory diarrhea.
What else to study on this topic
- The role of sialic acids in adsorption
- Mechanism of virion activation by GI tract proteases
- Functions of plus-strand RNA in translation
- Interaction of the virion with ER membranes
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