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Pathology of Viral  Hemorrhagic Fevers




Viral hemorrhagic fevers are a group of distinct acute viral infections that cause varying degrees hemorrhage and shock, and sometimes death.

There are many similar viral hemorrhagic fevers in different parts of the world, often named for the area where they are first described.

Viruses causing hemorrhagic fevers in man belong to the following virus groups:

Togavirus- Chikungunya ; Flavivirus  - Dengue ; Yellow  Fever ; Kyasanur Forest Disease ; Omsk hemorrhagic fever ; Arenavirus - Argentinian hemorrhagic fever ; Bolivian hemorrhagic fever ; Lassa Fever.

Filovirus-  Ebola Virus ; Marburg Virus.

Phlebovirus-  Rift Valley Fever.  ;

Nairovirus-   Crimean-Congo Hemorrhagic Fever  and

Hantavirus-  Hemorrhagic fever with renal syndrome.

Most hemorrhagic fever viruses are zoonoses, with the possible exception of the four dengue viruses, which may continually circulate among humans.

Hemorrhagic fever viruses are found in both temperate and tropical habitats and generally infect both sexes and all ages, although the age and sex of those infected are frequently influenced by the possibility of occupational exposure.

Transmission to humans is frequently by bite of an infected tick or mosquito or via aerosol from infected rodent hosts.

Aerosol and nosocomial transmission are especially important with Lassa, Junin, Machupo, Crimean-Congo hemorrhagic fever, Marburg, and Ebola viruses.

Seasonality of hemorrhagic fever among humans is influenced for the  most part by the dynamics of infected arthropod or vertebrate hosts.

Mammals, especially rodents, appear to be important natural hosts for many hemorrhagic fever viruses.

The transmission cycle for each hemorrhagic fever virus is distinct and is dependent upon the characteristics of the primary vector species and the possibility for its contact with humans.

Hemorrhagic fever virus infections can be approached by different therapeutic strategies:

(i) vaccination; (ii) administration of high-titred antibodies; and (iii) treatment with antiviral drugs.

Depending on the molecular target of their interaction, antiviral agents could be classified as follows:  IMP dehydrogenase inhibitors (i.e. ribavirin and its derivatives); OMP decarboxylase inhibitors (i.e.  pyrazofurin) ; CTP synthetase inhibitors (i.e. cyclopentylcytosine and cyclopentenylcytosine)   ; SAH hydrolase inhibitors (i.e.  neplanocin A)  ; polyanionic substances (i.e. sulfated polymers)  ; interferon and immunomodulators.


Further reading:

Pathogenesis of the viral hemorrhagic fevers.

Ebolavirus Entry Requires a Compact Hydrophobic Fist at the Tip of the Fusion Loop.

Rab18 Facilitates Dengue Virus Infection by Targeting Fatty Acid Synthase to Sites of Viral Replication.

Live Attenuated Tetravalent Dengue Virus Host Range Vaccine is Immunogenic in African Green Monkeys Following a Single Vaccination.

Animal Models for Viral Hemorrhagic Fever

Evaluation of complement system in children with Crimean-Congo hemorrhagic fever.

"Inhibitors of the tick-borne, hemorrhagic fever-associated flaviviruses."

High genetic diversity and adaptive potential of two simian hemorrhagic Fever viruses in a wild primate population.



Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)







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