Transmission of Hepatitis E Virus in Developing Countries

Abstract

Hepatitis E virus (HEV), an RNA virus of the Hepeviridae family, has marked heterogeneity. While all five HEV genotypes can cause human infections, genotypes HEV-1 and -2 infect humans alone, genotypes HEV-3 and -4 primarily infect pigs, boars and deer, and genotype HEV-7 primarily infects dromedaries. The global distribution of HEV has distinct epidemiological patterns based on ecology and socioeconomic factors. In resource-poor countries, disease presents as large-scale waterborne epidemics, and few epidemics have spread through person-to-person contact; however, endemic diseases within these countries can potentially spread through person-to-person contact or fecally contaminated water and foods. Vertical transmission of HEV from infected mother to fetus causes high fetal and perinatal mortality. Other means of transmission, such as zoonotic transmission, can fluctuate depending upon the region and strain of the virus. For instance, zoonotic transmission can sometimes play an insignificant role in human infections, such as in India, where human and pig HEV infections are unrelated. However, recently China and Southeast Asia have experienced a zoonotic spread of HEV-4 from pigs to humans and this has become the dominant mode of transmission of hepatitis E in eastern China. Zoonotic HEV infections in humans occur by eating undercooked pig flesh, raw liver, and sausages; through vocational contact; or via pig slurry, which leads to environmental contamination of agricultural products and seafood. Lastly, blood transfusion-associated HEV infections occur in many countries and screening of donors for HEV RNA is currently under serious consideration. To summarize, HEV genotypes 1 and 2 cause epidemic and endemic diseases in resource poor countries, primarily spreading through contaminated drinking water. HEV genotypes 3 and 4 on the other hand, cause autochthonous infections in developed, and many developing countries, by means of a unique zoonotic food-borne transmission.

Keywords: hepatitis E; hepatitis E virus; transmission; zoonosis.

Figure 1

Gulmarg Kashmir Epidemic, 1978–1979. Weekly occurrence of 20,083 hepatitis E cases reported from 200 villages (n = 600,000) from 4 September 1978 to 29 April 1979 (34 weeks). Epidemic curve lasted from the 8th to the 17th week (nine weeks). Prior to and following the epidemic, only isolated cases of hepatitis E were recorded, suggesting that person-to-person transmission was not of major consequence to the development of the epidemic.

Figure 2

Modes of transmission of hepatitis E in developing countries. The settings for contamination of drinking water have been drawn in sketches, with epidemics reported in each case.

Figure 3

Epidemic region: Kashmir, 1978. Drinking water is collected from a canal in which public latrine sewage flows, garbage of the whole locality is dumped, utensils and linen are washed, children swim, and locals buy fish (Adapted from Khuroo, et al. [4]).

Figure 4

Suggested model of repeated hepatitis E epidemics in hyperendemic areas. IgG anti-Hepatitis E virus (anti-HEV) positivity in the general population is around 4%. Following the epidemic, around 20% are sero-positive. There is a general decline in sero-positivity of IgG anti-HEV and poor exposure to HEV infections during the inter-epidemic period. Repeat outbreaks occur when sero-positivity is around 4% and there is gross fecal contamination of drinking water sources (Adapted from Khuroo, et al. [4]).

Figure 5

Zoonotic transmission of hepatitis E in developed and many developing countries.