Enterovirus 68 pathophysiology

Jump to navigation Jump to search

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

Enterovirus 68 Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Risk Factors

Differentiating Enterovirus 68 from other Diseases

Epidemiology and Demographics

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Ultrasound

Chest X Ray

CT Scan

MRI

Treatment

Medical Therapy

Surgery

Primary Prevention

Future or Investigational Therapies

Case Studies

Case #1

Enterovirus 68 pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Enterovirus 68 pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Enterovirus 68 pathophysiology

CDC on Enterovirus 68 pathophysiology

Enterovirus 68 pathophysiology in the news

Blogs on Enterovirus 68 pathophysiology

Directions to Hospitals Treating Enterovirus 68

Risk calculators and risk factors for Enterovirus 68 pathophysiology

Overview

Pathogenesis

Enterovirus 68 belongs to the Human Enterovirus D species (HEV-D), along with EV-70 and EV-94. Unlike the remaining, EV-69 is acid-labile, which reduces its ability to colonize the gastrointestinal mucosa. It has therefore been implicated in respiratory infections, and in rare occasions in CNS infection. This characteristic of EV-68 sets it apart from other enteroviruses, in what deals with its pathogenesis and infected cells.[1]

Besides cells of the respiratory mucosa, EV-68 also shows tropism for leukocytes, using the receptors that contain sialic-acid in these cells.[2] Since leukocytes are able to migrate to other tissues, by infecting these cells the virus gains access to secondary sites.[1] Viral replication inside leukocytes is likely to affect their function, thereby jeopardizing immune system response towards the virus, which facilitates its spread.[3]

EV-68 also replicates inside endothelial cells. By infecting these cells the virus is able to:[3]

However, EV-68 shows less tropism for endothelial cells than EV-70 or EV-94, which makes the secondary site infections less common for EV-68.[1]

Transmission

Due to being acid-labile, EV-68 is not shed in feces like other enteroviruses. Transmission of EV-68 is not as well-understood as those of other enteroviruses. EV-D68 causes respiratory disease, and the virus can be found in respiratory secretions such as saliva, nasal mucus, or sputum. The virus likely spreads from person to person when an infected person coughs, sneezes, or touches contaminated surfaces.

Life Cycle

References

  1. 1.0 1.1 1.2 Smura T, Ylipaasto P, Klemola P, Kaijalainen S, Kyllönen L, Sordi V; et al. (2010). "Cellular tropism of human enterovirus D species serotypes EV-94, EV-70, and EV-68 in vitro: implications for pathogenesis". J Med Virol. 82 (11): 1940–9. doi:10.1002/jmv.21894. PMID 20872722.
  2. Vlasak M, Roivainen M, Reithmayer M, Goesler I, Laine P, Snyers L; et al. (2005). "The minor receptor group of human rhinovirus (HRV) includes HRV23 and HRV25, but the presence of a lysine in the VP1 HI loop is not sufficient for receptor binding". J Virol. 79 (12): 7389–95. doi:10.1128/JVI.79.12.7389-7395.2005. PMC 1143622. PMID 15919894.
  3. 3.0 3.1 Kramer M, Schulte BM, Toonen LW, de Bruijni MA, Galama JM, Adema GJ; et al. (2007). "Echovirus infection causes rapid loss-of-function and cell death in human dendritic cells". Cell Microbiol. 9 (6): 1507–18. doi:10.1111/j.1462-5822.2007.00888.x. PMID 17298395.