Rotavirus

Jump to navigation Jump to search
style="background:#Template:Taxobox colour;"|Rotavirus
Electron micrograph of Rotaviruses.
Electron micrograph of Rotaviruses.
style="background:#Template:Taxobox colour;" | Scientific classification

Rotavirus infection Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Rotavirus infection from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Xray

CT scan

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Future or Investigational Therapies

Case Studies

Case #1

Rotavirus On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Rotavirus

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Rotavirus

CDC on Rotavirus

Rotavirus in the news

Blogs on Rotavirus

Directions to Hospitals Treating Rotavirus infection

Risk calculators and risk factors for Rotavirus

This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Rotavirus infection.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Rotaviruses are a genus of viruses belonging to the Reoviridae family. Seven major groups have been identified, three of which (groups A, B, and C) infect humans, with group A being the most common and widespread one. They cause vomiting and diarrhea and are the most common cause of severe diarrhea in children, killing about 600,000 children every year in developing countries (as of 2005). New vaccines have been shown to be safe and effective in 2006 [2].

Microbiology

One of Flewett's original electron micrographs
Computer reconstruction of a rotavirus particle
Rotavirus A from the faeces of an infected child

Structure

Rotaviruses have a genome consisting of 11 double-stranded RNA segments surrounded by a distinctive three-layered icosahedral protein capsid. The first layer is formed by the protein VP2, with each vertex having a copy of the proteins VP1 and VP3. The second layer is formed by the protein VP6. The outermost protein layer is composed of the structural glycoprotein VP7 and the spike protein VP4. Viral particles are up to 70nm in diameter and have a buoyant density of 1.36 g/ml in CsCl. By negative staining electron microscopy they resemble 'wheels' from which they derive their name (rota is Latin for wheel).

Cell Infection

Rotaviruses tend to affect gastrointestinal epithelial cells that are at the tip of the villus. Their triple protein coats make them very resistant to the normally prohibitive pH of the stomach, and also digestive enzymes (lipases and proteases) in the gastrointestinal tract.

When they infect a cell, they are ingested by the cell in endocytosis in a vesicle known as an endosome. Proteins in the third layer (VP7 and the VP4 spike) disrupt the membrane of the endosome, creating a difference in the Ca2+ concentration. This facilitates the breakdown of VP7 trimers into single protein subunits, leaving the VP2 and VP6 coats around the viral dsRNA, forming a double-layer particle (DLP).

While the eleven dsRNA strands are still within the protection of the two protein shells, RNA-dependent RNA polymerase creates viral mRNA transcripts of the double-stranded viral genome. This is more easily done within the environment in the "core" of the virus than in the host cell's aqueous environment, which significantly slows down the detachment of the two RNA strands to begin mRNA synthesis. Encapsidation of the viral RNA may also serve to evade host immune responses that are triggered by the presence of double-stranded RNA.

During the infection, rotavirus produces mRNA to support both protein translation and genome replication. Most of the rotavirus proteins accumulate in structures known as viroplasms, where the RNA is replicated and the DLPs are assembled. Viroplasms are electron-dense, perinuclear, punctate structures found as early as 2 hours after virus infection. Viroplasms are viral factories and are thought to be formed by two viral non-structural proteins, NSP5 and NSP2. Expression of certain forms of NSP5, especially one that is tagged at the NH2-terminus, results in the formation of viroplasms. Inhibition of NSP5 using intrabodies or RNA interference results in a profound decrease in rotavirus replication. The DLPs can migrate to the endoplasmic reticulum where they obtain their third, outer layer (formed by VP7 and VP4).

Transmission and associated foods

Rotaviruses are transmitted by the fecal-oral route. Person-to-person spread through contaminated hands is probably the most important means by which rotaviruses are transmitted in close communities such as pediatric and geriatric wards, day care centers and family homes.

Infected food handlers may contaminate foods that require handling and no further cooking, such as salads, fruits, and hors d'oeuvres. Rotaviruses are quite stable in the environment and have been found in estuary samples at levels as high as 1-5 infectious particles/gal. Sanitary measures adequate for bacteria and parasites seem to be ineffective in endemic control of rotavirus, as similar incidence of rotavirus infection is observed in countries with both high and low health standards.

The virus has not been isolated from any food associated with an outbreak, and no satisfactory method is available for routine analysis of food. However, it should be possible to apply procedures that have been used to detect the virus in water and in clinical specimens, of which reverse transcription (RT)-PCR amplification is the most sensitive method to food analysis.

Sources

See also

External links

References