Enterovirus 68 pathophysiology

Revision as of 15:24, 10 September 2014 by Joao Silva (talk | contribs)
Jump to navigation Jump to search

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

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

Unlike other enteroviruses, enterovirus 68 (EV-68) causes respiratory disease. Its cellular tropism, optimal growth at lower temperatures and acid-lability are responsible for infection of cells in the respiratory mucosa and leukocytes. The virus is able to replicate inside leukocytes, which allows it to infect the parenchymal tissue, to increase its viral load, spreading to other regions, and to activate endothelial cells, which attract more leukocytes to the infection site. The immune response towards the virus involves macrophages, B lymphocytes\B and T lymphocytes.

Pathogenesis

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

The virus shows optimal growth at lower temperatures, reason for what the respiratory tract constitutes and adequate region for viral replication. Besides the cells of the respiratory mucosa, EV-68 also shows tropism for leukocytes. For that it uses receptors on the lymphocyte surface containing sialic-acid.[2] Since leukocytes are capable 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, facilitating 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 secondary site infections less common in EV-68 infection.[1]

Immune Response

The immune response towards EV-68 is not fully understood. Viral clearance is achieved by an adequate T and B-cell response that contain and eliminate the virus. B lymphocytes, along with tissue macrophages contain the pathogen, while T lymphocytes penetrate the areas of infection, causing tissue damage. Tissue damage may lead to cell death of the affected areas.[4]

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 that 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.[5] Transmission of the virus was noted to occur more frequently between the months of August and November.[6]

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.
  4. Kreuter JD, Barnes A, McCarthy JE, Schwartzman JD, Oberste MS, Rhodes CH; et al. (2011). "A fatal central nervous system enterovirus 68 infection". Arch Pathol Lab Med. 135 (6): 793–6. doi:10.1043/2010-0174-CR.1. PMID 21631275.
  5. "Enterovirus D68".
  6. Lu QB, Wo Y, Wang HY, Wei MT, Zhang L, Yang H; et al. (2014). "Detection of enterovirus 68 as one of the commonest types of enterovirus found in patients with acute respiratory tract infection in China". J Med Microbiol. 63 (Pt 3): 408–14. doi:10.1099/jmm.0.068247-0. PMID 24324030.