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Rubella virus



Integumentary system


Rubella virus


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High Yield Notes
5 pages

Rubella virus

18 flashcards

USMLE® Step 1 style questions USMLE

1 questions

An 11-month-old girl is brought to the office by her parents for the evaluation of a rash. The patient had a low-grade fever for the past 2 days which was controlled with acetaminophen. Last night, the patient developed a pink rash on her face that has spread to her body this morning. The patient does not have cough, rhinorrhea, vomiting or diarrhea. The rest of the history is unremarkable. The patient has not received any vaccinations since birth. Temperature is 38.8°C (102°F), pulse is 98/min, respirations are 27/min, and blood pressure is 90/55 mmHg. Physical examination shows small tender lymph nodes in the suboccipital and postauricular region. Oropharyngeal examination is within normal limits. The rash is shown in the image.  

Reproduced from Wikipedia

Which of the following best describes the agent responsible for this patient’s condition?

External References

Content Reviewers:

Viviana Popa, MD


Alex Aranda

Rubella, the infection formerly known as “German Measles,'' is caused by the Rubella virus.

Thanks to vaccination, it’s a disease we see less and less, although because some groups are under-immunized, it’s still possible to see outbreaks.

The Rubella virus is part of the Togaviridae family.

Togaviruses are single-strand RNA viruses surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces, all within a spherical outer lipid envelope.

They’re also positive sense RNA viruses, which means that their genetic material is actually mRNA, so it can be used right away by the host cell to make viral proteins.

Now, the Rubella virus is transmitted through respiratory droplets, which are released into the environment when you sneeze or cough on another person.

Within the nasopharynx mucous membrane, the virus binds to a specific receptor on the membrane of epithelial cells.

It’s then surrounded by a little section of cell membrane that pinches off to form an endosome, that’s brought into the cell.

The low pH in the endosome uncoats the viral RNA and the virus causes changes to the endosome.

Now, when the Rubella virus enters the cell it also rearranges some of the organelles, gathering the endoplasmic reticulum, golgi apparatus, and mitochondria around the endosome.

The result is a membrane-bound Viral Replication Complex where - like the name says - the virus replicates.

So, after the virus replicates, its structural proteins are synthesized using the rough endoplasmic reticulum and these proteins are then transported to the golgi apparatus to be assembled and surrounded by membrane, a process called viral budding.

The new virus copy eventually exits the cell by exocytosis and enters nearby lymphatic and blood vessels, travelling to lymph nodes where it will replicate once again.

From the lymph nodes, it enters blood vessels again, and spreads to various parts of the body, making its way into various bodily fluids like urine, cerebrospinal fluid, and synovial fluid of joints.

Finally, the Rubella virus has a cytopathic, or cell-damaging, effect, that’s linked to viral replication.

This happens because the host body reacts to replication by causing apoptosis, or cell death, in infected cells, in an attempt to prevent the virus from spreading further.

Another way that Rubella can spread is from a pregnant female to her unborn child, through the placenta.

This causes Congenital Rubella Syndrome in the fetus. In fact, Rubella is among the most common infections that cause congenital defects in fetuses, which are grouped under the acronym TORCH. T stands for Toxoplasmosis, O for Other infections - like Syphilis, R for Rubella, C for Cytomegalovirus, and H for Herpes Simplex.

We’re not sure exactly how Rubella causes defects in the developing fetus but it’s possible that it causes vasculitis, or inflammation of blood vessels, which damages the vessels.

As a result, there’s not enough blood flow to developing organs which can result in tissue death.

It’s also possible that the Rubella virus slows down the process of mitosis, or cell division, in infected fetal cells.

Since mitosis helps drive the development of the fetus, infected tissues might not grow properly.

The timing of the infection in mom will determine the risk of the fetus also getting congenital Rubella.

Congenital defects are much more likely if the maternal infection happens between 4 weeks before and 20 weeks after conception.

After 20 weeks, there aren’t usually fetal defects, but there may be some intrauterine growth restriction, meaning the baby will be smaller than expected for their gestational age.

The biggest risk factor for Rubella is being unvaccinated—which is more common in countries with lower vaccination rates—and coming into contact with someone who is in the contagious period of their Rubella infection—which starts about 3 days after being exposed to the virus and lasts around 3 to 4 weeks.

Ok, now, many Rubella infections are asymptomatic, but when there are symptoms they typically show up after a 14 day incubation period.

Children tend to have fewer and milder symptoms which can last anywhere from 3 to 8 days on average.


Rubella virus is a single-strand, positive-sense RNA virus of the Togaviruses family, which is known to cause rubella, sometimes referred to as German measles. The virus is spread through respiratory droplets and infects and replicates in mucous membrane cells of the nasopharynx, then does the same in lymph nodes, triggering apoptosis in infected cells. Infected children are often asymptomatic or might have mild symptoms like fever, lymphadenopathy, and a rash, whereas adults tend to show more serious symptoms and get sick longer. Complications of rubella are rare but may include arthritis, encephalitis, and thrombocytopenia. Treatment for Rubella is supportive and prevention involves a live attenuated vaccine.