A Rbo Viruses

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R.Varidianto Yudo T., dr.,MKes

Lab. MikrobiologiFakultas Kedokteran Universitas Hang Tuah

Arboviruses


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The term arbovirus (arthropodborne virus)was originally used as a synonym fortogavirus.

The term "arbovirus" is an acronym for

arthropod-borne virus and highlights the factthat these viruses are transmitted byarthropods, primarily mosquitoes and ticks.

It is now no longer an official taxon since it

refers only to the arthropod vectors, whereasthe variety of virus types transmitted by thisroute is much greater, including for instancetogavirus as well as flavivirus types.


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The arboviruses are transmitted bybloodsucking arthropods from one vertebrate

host to another.

The vector acquires a lifelong infectionthrough the ingestion of blood from a viremic

vertebrate.

The viruses multiply in the tissues of the

arthropod without evidence of disease ordamage.

Some arboviruses are maintained in nature by

transovarian transmission in arthropods.


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Most arboviruses are classified in 2 Families,namely togaviruses and bunyaviruses

(1) Togaviruses are characterized by an

icosahedral nucleocapsidsurrounded by an

envelope and a single-stranded, positive-polarity

RNA genome.


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This family is subdivided into 4 genera on thebasis 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.


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(2) Bunyaviruses have a helical nucleocapsidsurrounded by an envelope and a genome

consisting of3 segments of negative-polarity RNA

that are hydrogen-bonded together.


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Classification of the major arboviruses

Family Genus Viruses of Medical

Interest

Togavirus Alphavirus Chikungunya, Eastern equine

encephalitis virus, Western

equine encephalitis virus,

Mayaro, O'Nyong-Nyong, Ross

River, Semliki Forest viruses.

Flavivirus Flavivirus Dengue virus, St. Louis

encephalitis virus, yellow fever

virus, West Nile virus

Bunyavirus Bunyavirus California encephalitis virus

Reovirus Orbivirus Colorado tick fever virus


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TRANSMISSION The life cycle of the arboviruses is based on

the ability of these viruses to multiply in boththe vertebrate host and the bloodsuckingvector.

For effective transmission to occur, the virusmust be present in the bloodstream of thevertebrate host (viremia) in sufficiently hightiter to be taken up in the small volume ofblood ingested during an insect bite.

After ingestion, the virus replicates in the gutof the arthropod and then spreads to otherorgans, including the salivary glands.


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Only the female of the species serves as thevector of the virus, because only she requiresa blood meal in order for progeny to beproduced.

An obligatory length of time called theextrinsic incubation period, must passbefore the virus has replicated sufficiently forthe 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.


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In addition to transmission through vertebrates,some arboviruses are transmitted by vertical"transovarian" passage from the mother tick toher offspring.

Vertical transmission has important survivalvalue for the virus if a vertebrate host isunavailable.

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 toolow and the duration of viremia too brief for thenext bite to transmit the virus.


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However, in some diseases, eg, yellow feverand dengue, humans have a high-level

viremia and act as reservoirs of the virus.

Infection by arboviruses usually does notresult in disease either in the arthropod vector

or in the vertebrate animal that serves as the

natural host.

Disease occurs primarily when the virusinfects dead-end hosts.


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CLINICAL FINDINGS &

EPIDEMIOLOGY

The diseases caused by arboviruses range in

severity from mild to rapidly fatal.

The clinical picture usually fits one of 3 categories:

1. Encephalitis

2. Hemorrhagic fever; or

3. Fever with myalgias, arthralgias, and

nonhemorrhagic rash


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The pathogenesis of these diseases involves notonly the cytocidal effect of the virus but also, in

some, a prominent immunopathologic

component.

Following recovery from the disease, immunity is

usually lifelong.


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DENGUE VIRUS Classic dengue ("breakbone fever") begins

suddenly with an influenzalike syndromeconsisting of fever, malaise, cough, andheadache.

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.


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In contras, dengue hemorrhagic feveris amuch more severe disease, with a fatality rate

that approaches 10%.

The initial picture is the same as classicdengue, but then shock and hemorrhage,

especially into the gastrointestinal tract and

skin, develop.

Dengue hemorrhagic fever occurs particularlyin southern Asia, whereas the classic form is

found in tropical areas worldwide.


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Hemorrhagic shock syndrome is due to theproduction of large amounts ofcross-reactingantibody at the time of a second dengue infection.

The pathogenesis is as follows: The patient recoversfrom classic dengue caused by one of the 4

serotypes, and antibody against that serotype isproduced.

When the patient is infected with another serotype ofdengue virus, an anamnestic, heterotypic responseoccurs 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, causingincreased vascular permeability andthrombocytopenia.

Shock and hemorrhage result.


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Dengue virus is transmitted by theAedesaegyptimosquito, which is also the vector ofyellow fever virus.

Human are the reservoir for dengue virus, but

a jungle cycle involving monkeys as thereservoir and otherAedes species as vectorsis suspected.

No antiviral therapy or vaccine for dengue isavailable.

Outbreaks are controlled by using insecticidesand draining stagnant eater that serves as thebreeding place for the mosquitoes.


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Properties of Flaviviruses

Flaviviruses show morphological uniformity with anicosahedral capsid and closefitting, spiked envelope.

The size of the capsid is about 30 nm and the wholevirion 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 nonstructuralproteins.

Both cotranslational and posttranslational protein

processing, similar to what is seen in the picornaviruses,has been described.

The morphogenesis of the virus occurs at theendoplasmic reticulum, into the lumen of which thefinished viruses bud.


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References 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 (22nded.). USA. Appleton & Lange

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