by Daniel Keays

Ka-dingo pepo

 

            The term viral hemorrhagic fever (VHF) is broad, with the keyword being hemorrhagic.  The bleeding is not caused by direct invasion of the virus but rather by a generalized disruption of the integrity of the vascular and coagulation systems brought on by an over-enthusiastic immune response.  The bleeding may be into the tissues or, in severe cases, escape from the body.  Such hemorrhages are a grave sign, and death usually ensues.  All viral hemorrhagic fever cases are acute.

            There are three main groups and one lesser group of viruses that can cause a case of hemorrhagic fever.  All are RNA viruses.  Ebola and Marburg viruses belong to the group known as the filoviruses, “filo” coming from the Latin filum, or thread, because of their appearance under the electron microscope.

            A second major group is the flaviviruses, from the Latin flavus, meaning “yellow.”  The name comes from the common name for one disease caused by the group, yellow fever.  This group has many members, the most recognizable being yellow fever, dengue, West Nile, and Zika.  There are over 60 different flaviviruses in all.  All are carried by insects, primarily mosquitoes, some by ticks, so the name often applied is “arbovirus,” or arthropod-borne virus.  Yellow fever and dengue most likely crossed the Atlantic to the Americas during the slave trade, while West Nile and Zika may have crossed the ocean on a modern-day jet airliner.  

A third virus group responsible for acute hemorrhagic fevers is known collectively as the Bunyavirus family.  Some of the more generally recognized members of the group are the Crimean-Congo virus, Rift Valley Fever virus, La Crosse, and Hantavirus.  All are associated with rodents and are transmitted by insects, usually mosquitoes and ticks.  The name Bunyavirus comes from Bunyamwera, an area in Western Uganda where the virus was first isolated in the early 1940s.  While not as prevalent as the flaviviruses, the Bunyaviruses can also cause severe disease, including viral hemorrhagic fever.

            The arenaviruses are the fourth group of viruses capable of producing hemorrhagic fevers in humans.  They are rare, usually associated with rodent droppings, and apparently not transmissible human-to-human.  Like the other hemorrhagic fever viruses, they greatly reduce the amount of interferon the infected host produces.  Lassa fever virus is the most well-known of the arenaviruses.

 

Dengue.  Dengue (pronounced deng-y, the u is silent) is a potentially severe ailment observed in many world areas.  It’s been found in over 100 countries.  The name probably comes from the Swahili term for it, “Ka-dingo pepo,” meaning “cramp-like seizure caused by an evil spirit.”  It may be that Spanish explorers adopted the name from that.   A vivid name for the disease is attributed to American physician Benjamin Rush in the 1780s, who used the descriptive moniker “break-bone fever.”  The muscle and joint pain can be so severe that it feels like your bones may break. 

            Clinically, dengue is an odd disease.  Odd in that when the virus first infects a person, they usually don’t become very ill.  They may have a little discomfort, but it is often not enough to seek medical advice.  The real trouble begins after a second infection.  The severe symptoms are a result of an over-vigorous immune response.

            There are four different types of the dengue virus.  Types 1 and 2 predominate.  The virus infects the cells of the mosquito that carries it, Aedes aegypti.  Aedes has two features that make it especially troublesome.  It is “domesticated” in the sense that it is well adapted to humans and our environment.  The other is that it is an active feeder during the day, so many people are potentially exposed to bites.  

            Dengue virus makes ten proteins.  Three are on the surface, giving the virus its structural integrity.   The other seven are non-structural and located in the virus's interior.  One of these non-structural proteins, NS-1, is responsible for many people's severe reactions after getting infected.

            The virus releases NS-1 during infection.  It gets into the bloodstream and circulates throughout the body.  It has a strong affinity for the cells of the endothelium lining of blood vessels and attaches to them.  Upon the first infection, the immune response to the virus is typical: antibodies are made to the proteins making up the viral core and the free-floating NS-1 protein.  The virus and NS-1 are cleared in a short time, usually without much harm to the patient.

            Trouble occurs when the patient is infected a second time with another type of the virus.  Say the initial infection was with type 1.  Antibodies are made to its core proteins as well as to NS-1.  If the individual is infected a few years later with type 2, the immune reaction to the core proteins is a matter of routine; antibodies to type 1 do not protect against type 2.  But the NS-1 proteins of types 1 and 2 are antigenically the same, so the immune system is locked and loaded to react to NS-1.  The problem is that there is so much NS-1 produced during the second infection, and the immune system is primed to take it out, and there is a tremendous immune overreaction.  NS-1 is attached to the inner lining of blood vessels, and antibodies bind to it at that place.  The result is a deterioration in the integrity of the blood vessel lining with resultant leakage.  As in Ebola infection, the result is sometimes viral hemorrhagic fever, a very serious condition.

            The range of symptoms displayed in a dengue infection is wide.  Many patients display mild to moderate reactions, but some are severely affected.  The genetics of both the patient and the microbe, the strain of the virus, the timing of the initial infection, and the amount of virus injected by the mosquito all play a role. 
 

Aedes aegytpti

(Photo from Public Health Image Library, CDC)

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