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R.Varidianto Yudo T., dr.,MKes

Lab. Mikrobiologi Fakultas Kedokteran Universitas Hang Tuah

The term arbovirus (arthropodborne virus)

was originally used as a synonym for togavirus. The term "arbovirus" is an acronym for arthropod-borne virus and highlights the fact that these viruses are transmitted by arthropods, primarily mosquitoes and ticks. It is now no longer an official taxon since it refers only to the arthropod vectors, whereas the variety of virus types transmitted by this route is much greater, including for instance togavirus as well as flavivirus types.

The arboviruses are transmitted by

bloodsucking arthropods from one vertebrate host to another. The vector acquires a lifelong infection through the ingestion of blood from a viremic vertebrate. The viruses multiply in the tissues of the arthropod without evidence of disease or damage. Some arboviruses are maintained in nature by transovarian transmission in arthropods.

Most arboviruses are classified in 2 Families,

namely togaviruses and bunyaviruses (1) Togaviruses are characterized by an icosahedral nucleocapsid surrounded by an envelope and a single-stranded, positive-polarity RNA genome.

This family is subdivided into 4 genera on the

basis of size and antigenic relationships:

alphaviruses (60- 70 nm) rubiviruses (60- 70 nm) flaviviruses (45-55 nm) It became family !!

pestiviruses (45-55 nm).

Only alphaviruses and flaviviruses are

considered here. The only rubivirus is rubella virus and pestiviruses do not cause human disease.

(2) Bunyaviruses have a helical nucleocapsid

surrounded by an envelope and a genome consisting of 3 segments of negative-polarity RNA that are hydrogen-bonded together.

Classification of the major arboviruses

Family Togavirus Genus Alphavirus Viruses of Medical Interest Chikungunya, Eastern equine encephalitis virus, Western equine encephalitis virus, Mayaro, O'Nyong-Nyong, Ross River, Semliki Forest viruses. Dengue virus, St. Louis encephalitis virus, yellow fever virus, West Nile virus California encephalitis virus Colorado tick fever virus



Bunyavirus Bunyavirus Reovirus Orbivirus

The life cycle of the arboviruses is based on

the ability of these viruses to multiply in both the vertebrate host and the bloodsucking vector. For effective transmission to occur, the virus must be present in the bloodstream of the vertebrate host (viremia) in sufficiently high titer to be taken up in the small volume of blood ingested during an insect bite. After ingestion, the virus replicates in the gut of the arthropod and then spreads to other organs, including the salivary glands.

Only the female of the species serves as the

vector of the virus, because only she requires a blood meal in order for progeny to be produced. An obligatory length of time called the extrinsic incubation period, must pass before the virus has replicated sufficiently for the saliva of the vector to contain enough virus to transmit an infectious dose. For most viruses, the extrinsic incubation period ranges from 7 to 14 days.

In addition to transmission through vertebrates,

some arboviruses are transmitted by vertical "transovarian" passage from the mother tick to her offspring. Vertical transmission has important survival value for the virus if a vertebrate host is unavailable. Humans are involved in the transmission cycle of arboviruses in 2 different ways. Usually, humans are "dead-end" hosts, because the concentration of virus in human blood is too low and the duration of viremia too brief for the next bite to transmit the virus.

However, in some diseases, eg, yellow fever

and dengue, humans have a high-level viremia and act as reservoirs of the virus. Infection by arboviruses usually does not result in disease either in the arthropod vector or in the vertebrate animal that serves as the natural host. Disease occurs primarily when the virus infects dead-end hosts.


The diseases caused by arboviruses range in severity from mild to rapidly fatal. The clinical picture usually fits one of 3 categories:
1. 2. 3.

Encephalitis Hemorrhagic fever; or Fever with myalgias, arthralgias, and nonhemorrhagic rash

The pathogenesis of these diseases involves not

only the cytocidal effect of the virus but also, in some, a prominent immunopathologic component. Following recovery from the disease, immunity is usually lifelong.

Classic dengue ("breakbone fever") begins

suddenly with an influenzalike syndrome consisting of fever, malaise, cough, and headache. Severe pains in muscles and joints (breakbone) occur. Enlarged lymph nodes, a maculopapular rash, and leukopenia are common. After a week or so, the symptoms regress but weakness may persist. Although unpleasant, this typical form of dengue is rarely fatal and has few sequelae.

In contras, dengue hemorrhagic fever is a

much more severe disease, with a fatality rate that approaches 10%. The initial picture is the same as classic dengue, but then shock and hemorrhage, especially into the gastrointestinal tract and skin, develop. Dengue hemorrhagic fever occurs particularly in southern Asia, whereas the classic form is found in tropical areas worldwide.

Hemorrhagic shock syndrome is due to the

production of large amounts of cross-reacting antibody at the time of a second dengue infection. The pathogenesis is as follows: The patient recovers from classic dengue caused by one of the 4 serotypes, and antibody against that serotype is produced. When the patient is infected with another serotype of dengue virus, an anamnestic, heterotypic response occurs and large amounts of cross-reacting antibody to the first serotype are produced. Immune complexes composed of virus and antibody are formed that activate complement, causing increased vascular permeability and thrombocytopenia. Shock and hemorrhage result.

Dengue virus is transmitted by the Aedes

aegypti mosquito, which is also the vector of yellow fever virus. Human are the reservoir for dengue virus, but a jungle cycle involving monkeys as the reservoir and other Aedes species as vectors is suspected. No antiviral therapy or vaccine for dengue is available. Outbreaks are controlled by using insecticides and draining stagnant eater that serves as the breeding place for the mosquitoes.

Properties of Flaviviruses
Flaviviruses show morphological uniformity with an

icosahedral capsid and closefitting, spiked envelope. The size of the capsid is about 30 nm and the whole virion measures 45 nm. The genome of the flaviviruses is a single stranded, (+) sense RNA about 10 kb in size. It codes for three structural and seven nonstructural proteins. Both cotranslational and posttranslational protein processing, similar to what is seen in the picornaviruses, has been described. The morphogenesis of the virus occurs at the endoplasmic reticulum, into the lumen of which the finished viruses bud.

Levinson W, 2004. Medical Microbiology &

Immunology: Examination & Board Review, Eighth Edition. McGraw-Hill Companies, Inc., USA Brooks G.F., Butel J.S., Morse S.A., 2001. Jawetz, Melnick and Adelbergs Medical Microbiology (22nd ed.). USA. Appleton & Lange