Rubella virus

17,398views

Rubella virus

INFD

INFD

Viral structure and functions
Poliovirus
Rotavirus
Adenovirus
Parvovirus B19
Coxsackievirus
Rhinovirus
Influenza virus
Norovirus
Rabies virus
Hepatitis A and Hepatitis E virus
Hepatitis D virus
Human parainfluenza viruses
Respiratory syncytial virus
Hepatitis C virus
Coronaviruses
Poxvirus (Smallpox and Molluscum contagiosum)
Human papillomavirus
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Mumps virus
Measles virus
Rubella virus
Varicella zoster virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Dengue virus
Zika virus
West Nile virus
Yellow fever virus
Ebola virus
Eastern and Western equine encephalitis virus
Lymphocytic choriomeningitis virus
Hantavirus
HIV (AIDS)
Human T-lymphotropic virus
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Herpesvirus medications
Mycobacterium leprae
Mycobacterium avium complex (NORD)
Mycoplasma pneumoniae
Bacterial structure and functions
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Mycobacterium tuberculosis (Tuberculosis)
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium tetani (Tetanus)
Clostridium difficile (Pseudomembranous colitis)
Bacillus cereus (Food poisoning)
Bacillus anthracis (Anthrax)
Cell wall synthesis inhibitors: Penicillins
Antituberculosis medications
Cell wall synthesis inhibitors: Cephalosporins
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus agalactiae (Group B Strep)
Streptococcus pyogenes (Group A Strep)
Enterococcus
Treponema pallidum (Syphilis)
Borrelia species (Relapsing fever)
Borrelia burgdorferi (Lyme disease)
Leptospira
Protein synthesis inhibitors: Aminoglycosides
Protein synthesis inhibitors: Tetracyclines
Miscellaneous cell wall synthesis inhibitors
Miscellaneous protein synthesis inhibitors
DNA synthesis inhibitors: Metronidazole
Corynebacterium diphtheriae (Diphtheria)
Actinomyces israelii
Bacteroides fragilis
Yersinia pestis (Plague)
Moraxella catarrhalis
Neisseria gonorrhoeae
Neisseria meningitidis
Chlamydia pneumoniae
Chlamydia trachomatis
Klebsiella pneumoniae
Proteus mirabilis
Escherichia coli
Salmonella (non-typhoidal)
Pseudomonas aeruginosa
Salmonella typhi (typhoid fever)
Enterobacter
Shigella
Helicobacter pylori
Vibrio cholerae (Cholera)
Campylobacter jejuni
Bordetella pertussis (Whooping cough)
Haemophilus influenzae
Haemophilus ducreyi (Chancroid)
Pasteurella multocida
Francisella tularensis (Tularemia)
Brucella
Coxiella burnetii (Q fever)
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Ehrlichia and Anaplasma
Coccidioidomycosis and paracoccidioidomycosis
Histoplasmosis
Blastomycosis
Pneumocystis jirovecii (Pneumocystis pneumonia)
Candida
Mucormycosis
Aspergillus fumigatus
Sporothrix schenckii
Cryptococcus neoformans
Plasmodium species (Malaria)
Babesia
Giardia lamblia
Entamoeba histolytica (Amebiasis)
Cryptosporidium
Acanthamoeba
Naegleria fowleri (Primary amebic meningoencephalitis)
Toxoplasma gondii (Toxoplasmosis)
Trypanosoma brucei
Trypanosoma cruzi (Chagas disease)
Trichomonas vaginalis
Leishmania
Loa loa (Eye worm)
Toxocara canis (Visceral larva migrans)
Onchocerca volvulus (River blindness)
Ascaris lumbricoides
Anisakis
Angiostrongylus (Eosinophilic meningitis)
Ancylostoma duodenale and Necator americanus
Strongyloides stercoralis
Guinea worm (Dracunculiasis)
Wuchereria bancrofti (Lymphatic filariasis)
Trichinella spiralis
Enterobius vermicularis (Pinworm)
Trichuris trichiura (Whipworm)
Echinococcus granulosus (Hydatid disease)
Diphyllobothrium latum
Paragonimus westermani
Clonorchis sinensis
Schistosomes
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
HIV and AIDS: Pathology review
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Impetigo

Transcript

Watch video only

Content Reviewers

Contributors

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.

Key Takeaways

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.