Measles pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:  Guillermo Rodriguez Nava, M.D. [2]

## Overview[edit | edit source]

Measles is caused by a nonsegmented negative-stranded RNA virus of the Paramyxoviridae family, genus Morbillivirus. The primary site of infection is the respiratory epithelium of the nasopharynx and it is transmitted in respiratory secretions, via aerosol droplets containing virus particles.

## Pathogenesis[edit | edit source]

* Measles is a systemic infection.[1]
* The primary site of infection is the respiratory epithelium of the nasopharynx.
* Cellular receptors: CD46 (ubiquitous) and CD150 (antigen-presenting cells and lymphocytes).[2]
* Two to three days after invasion and replication in the respiratory epithelium and regional lymph nodes, a primary viremia occurs with subsequent infection of the reticuloendothelial system.
* Following further viral replication in regional and distal reticuloendothelial sites, a second viremia occurs 5–7 days after initial infection.
* During this viremia, there may be infection of the respiratory tract and other organs.
* Measles virus is shed from the nasopharynx beginning with the prodrome until 3–4 days after rash onset.
* The symptoms are caused by the immune response.
* At the acute phase of the infection, the IL-2 drives the immune response to a stronger Th1 response and cellular T-cell CD8 response, which is vital for viral elimination. [3][4]
* Later on, the secretion of IL-4 and IL-10 rises, driving the immune response to a stronger Th2 response and inhibiting the Th2 response respectively, which allows the development of measles virus-specific antibodies and establishment of long-term immunity.[3]
* The measles infection induces immunosuppression in the host even months after the resoluton of the infection, predisposing the host to other infections.[5]
* Alterations on the immune response include[5]:
* Lymphopenia
* Suppression of cellular immunity
* Inhibition of multiplication of periphereal blood lymphocytes

## Transmission[edit | edit source]

* The measles is a highly contagious airborne pathogen which spreads primarily via the respiratory system.
* The virus is transmitted in respiratory secretions, and can be passed from person to person via aerosol droplets containing virus particles, such as those produced by a coughing patient.
* The virus resides in the mucus in the nose and throat of the infected person. When that person sneezes or coughs, droplets spray into the air. The infected mucus can land in other people’s noses or throats when they breathe or put their fingers in their mouth or nose after handling an infected surface.
* The virus remains active and contagious on infected surfaces for up to 2 hours. Measles spreads so easily that anyone who is not immunized will probably get it, eventually.
* Once transmission occurs, the virus infects the epithelial cells of its new host, and may also replicate in the urinary tract, lymphatic system, conjunctivae, blood vessels, and central nervous system.[6]
* It spreads through respiration (contact with fluids from an infected person's nose and mouth, either directly or through aerosol transmission), and is highly contagious-- 90% of people without immunity sharing a house with an infected person will catch it.
* Airborne precautions should be taken for all suspected cases of measles.
* The incubation period usually lasts for 4-12 days (during which there are no symptoms).
* Infected people remain contagious from the appearance of the first symptoms until 3-5 days after the rash appears.
* German measles is an unrelated condition caused by the rubella virus.
* Humans are the only known natural hosts of measles, although the virus can infect some non-human primate species.

## References[edit | edit source]

1. ↑ "Measles: Epidemiology and Prevention of Vaccine-Preventable Diseases".
2. ↑ Yanagi Y, Takeda M, Ohno S (2006). "Measles virus: cellular receptors, tropism and pathogenesis". J Gen Virol. 87 (Pt 10): 2767–79. doi:10.1099/vir.0.82221-0. PMID 16963735.CS1 maint: Multiple names: authors list (link)
3. ↑ 3.0 3.1 Naniche D (2009). "Human immunology of measles virus infection". Curr Top Microbiol Immunol. 330: 151–71. PMID 19203109.
4. ↑ Griffin DE (2010). "Measles virus-induced suppression of immune responses". Immunol Rev. 236: 176–89. doi:10.1111/j.1600-065X.2010.00925.x. PMC 2908915. PMID 20636817.CS1 maint: PMC format (link)
5. ↑ 5.0 5.1 Avota E, Gassert E, Schneider-Schaulies S (2010). "Measles virus-induced immunosuppression: from effectors to mechanisms". Med Microbiol Immunol. 199 (3): 227–37. doi:10.1007/s00430-010-0152-3. PMID 20376484.CS1 maint: Multiple names: authors list (link)
6. ↑ Flint SJ, Enquist LW, Racaniello VR, and AM Skalka. Principles of Virology, 2nd edition: Molecular Biology, Pathogenesis, and Control of Animal Viruses. Text " 2004" ignored (help)CS1 maint: Multiple names: authors list (link)

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