In this article we will discuss about Arbo Viruses:- 1. Introduction to Arbo Viruses 2. Classification of Arbo Viruses 3. General Properties.
Introduction to Arbo Viruses:
The arthropod viruses or Arbo viruses are a group of RNA viruses of diverse physical and chemical properties, that are transmitted by blood sucking arthropod from one vertebrate host to another. The viruses multiply in arthropods without producing disease vectors acquire lifelong infection.
The Rodent-borne (robo) viruses are maintained in nature by direct transmission from rodent to rodent by contact of body fluids or excretions of infected rodents. It is not transmitted by Arthropods.
Robo viruses consist of the arena viruses of the family Arena viridae (Zoonotic in rodents).
Classification of Arbo Viruses:
Arbo viruses were designated according to the disease with which they are associated e.g. Yellow fever, Rift valley fever, Chikungunya and Kyasanur Forest disease. Sometimes they were named after the geographic area e.g. St. Louis encephalitis and West Nile fever.
They contain about 450 viruses and infect man, mammal, bird, snake.
They include five families:
Togaviridae, Flaviviridae, Bunyaviridae, Reoviridae, Rhabdoviridae. Togaviruses of medical importance are Alpha virus and Rubi virus.
1. Alpha Viruses:
They attach to the receptors of host cells by means of E1 and E2 glycoproteins of envelope and by endocytosis they enter into host cells. The single stranded RNA genome may act as messenger molecule release of virus occurs by budding from cell membrane.
Twenty five serotypes of alpha viruses are mosquito-borne:
(A) Encephalitis Viruses:
Western, Eastern and Venezuelan encephalitis viruses are three important strains producing encephalitis in horses and men. Wild birds are reservoirs of viruses that are transmitted by Culex and Anopheles mosquitoes.
(B) Viruses Causing Febrile Illness:
i. Chikungunya Virus:
The name is derived from the which language native word for “double up” which occurs in the disease due to severe joint pain. The term was first coined by the people of Makonde Tribe in Tanzania, Africa in their native language. This virus produces only a viraemia phase characterised by fever, creeping joint pain and rash and is transmitted by Aedes aegypti.
Epidemics of chikungunya virus infection have been reported from Africa, Thailand (1958) and India (1963, Kolkata and Chennai) along East coast of India and Maharashtra, the disease was endemic till 1975.
ii. Semiliki Forest Virus:
In 1942 this virus was first isolated in Semiliki forest of Uganda from Aedes mosquitoes and it is pathogenic for mice, not for man, although neutralizing antibodies to this virus are detected in serum of African people.
iii. Sindbis Virus:
In 1952, this virus was first recovered from Culex mosquitoes in Sindbis district of Egypt. Febrile illness in man was caused by this virus in Philippines, Australia and India.
2. Flavi Viruses:
They are similar to alpha viruses in many respects, but they differ by the composition of envelope glycoprotein and RNA. Out of 60 serotypes some are mosquito-borne, others are tick-borne:
(A) Mosquito-Borne Flavi Viruses:
i. Encephalitis Viruses:
In this group, there are five viruses which cause encephalitis and are named after the geographical zones. St. Louis encephalitis virus (North and Central America); Ilheus virus (South and Central America); West Nile virus (West Nile province of Uganda), Murray valley encephalitis virus (Australia and New Guinea) and Japanese B encephalitis virus. These viruses are transmitted by Culex mosquitoes.
Japanese B Encephalitis (JBE) Viruses:
This (JBE) virus was so named to distinguish it from Japanese A encephalitis virus which was prevalent at that time. It was first reported in Japan in 1935; later, in South East Asia, Korea, Malaysia and India, it caused most serious illness.
Pathogenesis of Mosquito-Borne Flavi Viruses:
This JBE virus spreads from bird to bird through Culex tritaeniorhynchus. Human infection occurs from herons (reservoir) by several species of Culicidae mosquitoes. The disease was first recognised in Tamil Nadu in 1955 during an outbreak of encephalids.
In Tamil Nadu (India) the JBE occurs during June to October. Several outbreaks of JBE have been reported in different parts of India—Bankura and Burdwan of West Bengal, Dibrugarh in Assam, Uttar Pradesh, Goa, Karnataka.
Clinical Features of Mosquito-Borne Flavi Viruses:
JBE has a sudden onset, with fever and vomiting. After an incubation period of 1-6 days, shows signs of encephalitis—neck rigidity, convulsions, drowsiness, deepening coma, neurological signs (paralysis, tremor).
All parts of CNS (basal structures of brain, cerebral cortex- spinal cord) are involved. Perivascular cuffing and mononuclear cell infiltration of meanings are common. Acute phase lasts for about two weeks. Mortality rate is 50% in some epidemics. Convalescence may last for many weeks; paralysis (residual) persists in about 50% survivors.
Prevention of Mosquito-Borne Flavi Viruses:
The spread of this disease can be prevented by the control of mosquitoes and taking away piggeries from the residential areas. A formalin in activated vaccine is useful for the pigs during epidemics.
ii. Yellow Fever:
It is an acute febrile illness transmitted by mosquito. Rapid and extensive destruction of liver can be seen in severe cases.
Incubation period is 3-6 days and this illness occurs in two forms:
“Urban cycle“—where man is the reservoir and Aedes aegypti is the vector; Forest or Sylvatic cycle—where wild monkeys act as reservoirs, forest mosquitoes as vectors.
In many countries, yellow fever is still endemic. In India, it does not exist due to strict vigilance on vaccination and quarantine of travellers from other countries (endemic areas). Attenuated live vaccine of 17 D strain is protective against yellow fever.
iii. Dengue:
This infection is also transmitted by Aedes mosquito and is characterised by the sudden onset of fever, headache, pain in bone joints and muscles. Hence it is called “break-bone fever“. Lymphadenopathy and maculopapular rash.
Though endemic, is often epidemic in tropical and subtropical countries (India, South East Asia, Pacific Islands). In East Coast of India, dengue is common. There are four serological subtypes of Dengue virus (1-4). Though Dengue and Yellow fever are antigenically related, there is no cross-immunity.
Clinical features of Mosquito-Borne Flavi Viruses:
Clinically, the disease is manifested in two forms:
(a) Classical dengue fever has relatively benign course with fever, headache, pain in muscle and bones. Incubation period is 5-8 days. Rash may appear on 3rd or 4th day. Febrile illness lasts for about a week and terminates by crisis. It is rarely fatal.
(b) Dengue haemorrhagic fever appear to be a hyper-immune response and is seen in patients previously infected with dengue fever virus. On reinfection with a different strain of virus within a period of 2 years of first infection, antibodies formed against the first virus reacts with the second subtype forming immune complex (virus-antibody complex).
Initial symptoms are associated with haemorrhagic rash, thrombocytopenia and shock. The mortality rate is 5-10%. Type 2 dengue virus is often responsible for the haemorrhagic fever. The disease is epidemic in Thailand, South East Asia and India, where dengue serotypes are present. The disease can be controlled by anti-mosquito measures. No effective vaccine is available.
(B) Tick-borne Flavi viruses:
i. Tick-borne encephalitis virus:
Russian spring summer encephalitis (RSSE) has been reported in Central, Eastern Europe, CIS countries. The ticks are the vectors and the bats are reservoirs. Infected goats excrete the virus in the milk. Clinically, patient develops ascending paralysis and hemi-paralysis with 30% mortality.
Control can be conducted:
1. By avoiding tick-bite
2. By formalin inactivated RSSE.
Vaccine for Flavi Viruses:
In North USA, Canada, Powssan virus can cause Powssan encephalitis.
ii. Tick-borne Haemorrhagic Fever:
(a) Kyasanur Forest Disease (KFD) is an Indian haemorrhagic disease appeared, in 1957, in Kyasanur forest of Karnataka (India) and is caused by a virus which is antigenically related to RSSE and isolated in National Institute of Virology, Pune (India). This KFD virus affects haemopoietic system. Birds and small mammals are reservoirs of the virus which is transmitted by the bite of tick (Haemaphysalis spinigera).
Clinical Features Tick-Borne Flavi Viruses:
Incubation period is 3-7 days. KFD is characterised by sudden onset of fever with headache, vomiting, myalgia, severe prostration. Massive haemorrhage in alimentary canal, chest cavity and epistaxis may occur in some cases. The fatality is about 10%.
Epidemiology of Tick-Borne Flavi Viruses:
KFD virus is responsible for the natural infection in langur and bonnet monkeys; then in man in South and Western India (Shimoga district of Karnataka, Kutch and Saurashtra). A killed vaccine is found to be satisfactory in field trial.
(b) Omsk haemorrhagic fever has been reported in CIS countries,-Rumania. The virus is related to KFD and causes clinical symptoms similar to KFD.
3. Buniya Viruses:
They are larger than alpha and flavi viruses and their nucleic acid genome contains three molecules (M, S and L strands) of circular single stranded RNA. The virus contains an RNA. The name of this virus family (Bunya-viridae) is derived from a place Bunyamvera in Uganda of Africa from where this virus was first isolated.
Virology:
They are spherical (901-00 nm) particles, replicate in cytoplasm and enveloped. They contain single stranded RNA genome which is trisegmented.
Classification of Buniya Viruses:
California Group:
1. California encephalitis virus was first isolated from mosquitoes in 1942 in California.
2. la Crossie virus was isolated in Wisconsin (USA).
3. Chitor virus was isolated in Chitor (India).
All three viruses are antigenically related and similar in clinical features except that Chitoor virus causes mild fever. Clinically, there is fever, headache and mild or severe central nervous system involvement. All infections are mosquito-borne and are more common among children. Recovery is usually complete with rare fatality.
Phlebo Virus Group:
i. Sand Fly Fever (Phlebotomous Fever):
It is transmitted by female sand fly (Phlebotomous papatasi). After an incubation period of 3-5 days, patient develops fever, malaise, headache, and nausea which lasts for 3- 4 days. This infection has been reported in India, Pakistan, Central Asia and Mediterranean countries. Sand flies breed in sand, dust and soil.
Phlebotomous virus has two serological types:
Sicily and Naples strains.
Chandipura Virus:
This Chandipura belongs to same family as Rabies virus. This rare virus was first found at Chandipura in Northern Maharashtra (India) in 1965—called as killer virus claiming 108 children—though it had spread in epidemic form in Andhra Pradesh killing 165 children in 2003.
The killer virus with a very high fatality rate of 60 per cent had made-its appearance in Gujarat for the first time claiming lives of 16 children and affecting at least 26 others in Chota Udaipur and Kwant talukas in the year 2004. Chandipura is the name of first patient.
In view of similar symptoms found in Andhra Pradesh, National Institute of Virology (NIV), Pune (India), suggested that this causative organism could be Chandipura virus’ and its mode of transmission was through sand flies which are vectors carrying virus. This deadly virus earlier, it was suspected, as virus causing Japanese encephalitis—a disease endemic to Asia.
Studies on the vector population and symptoms ruled out the possibility of viral encephalitis. Most children developed dramatic symptoms as the disease progressed much faster than normal—from chills, fever, vomiting and convulsions to coma and death.
Treatment of Buniya Viruses:
Since there is no definite cure, the patients were given supportive treatment.
Prevention and control of Buniya Viruses:
Luckily 11 sand flies (vectors) are susceptible to pesticides, they can be eradicated by spraying the insecticides.
ii. Rift Valley Fever:
It is mainly a disease in sheep and other domestic animals in Rift Valley (Kenya) and Middle East. Human beings are secondarily infected during epizootics in domestic animals. The clinical features resemble influenza-like illness and dengue fever.
Nairo Sheep Disease Virus:
In Equatorial Africa this virus causes economic loss in sheep. Ganjam virus caused a disease in India in sheep. It is related to Nairo virus. Haemaphysalis tick is the vector. The Nairo virus sometimes infects man causing haemorrhagic fever.
Orbi Virus:
Three genera—Reo virus, Orbi virus and Rota virus belong to the family Reoviridae. Arthro borne infection is caused by Orbi virus only. In the genus, Orbi virus, only Colorado tick borne virus is recognised pathogen which is maintained in wild rodent population; it is spread by wood tick, Dermacenter Anderson. This illness is characterised by a mild fever and it is self-limited in Western USA.
Vesiculo Virus:
In 1967, Chandipura virus was isolated in Nagpur (India) from blood of patients during dengue-chikungunya fever. The pathogenic role is not yet well-understood. Sand-flies and Aedes aegypti are the vectors in which Chandipura virus multiplies.
Rodent-Borne Haemorrhagic Fevers:
Arena Viridae:
Arena (aeronostis, Latin for sandy) viruses are of grainy appearance of virions under electron microscope. They are spherical, 85-120 nm diameter and contain single stranded segmented RNA genome. They are maintained in nature in rodent without the help of arthropod vectors.
Man gets the infection by contact with excreta (urine and faeces) of infected rodents. Clinical features are fever, petechiae, or purpura, gastrointestinal, nasal and uterine bleeding, leucopenia, thrombocytopenic and shock. Central nervous system involvement may often terminate into death.
Filo Virus:
This virus does not belong to Arbo virus group, but they are described under Arbo virus group as they have similar clinical features. Marburg virus and Ebola virus are two members of Filoviridae and are enveloped, tubular (800-1500 x 80 nm) and contain single stranded RNA genome. They possess 7 nm surface spikes. The incubation period is 3-10 days. These viruses cause acute febrile haemorrhagic fever.
(i) The Marbug virus was first isolated in Marburg, Germany, and Yugoslavia. Fatality rate was about 35%. This virus was epidemiologically linked to monkeys imported from the same area and was isolated from blood and tissue of these monkeys. Infection may be due to accidental needle sticks or abrasions. This virus was demonstrated in the semen of one patient and is grown in vero cell.
(ii) Ebola virus was first described in 1977 following an outbreak of haemorrhagic fever in Southern Sudan and Northern Zaire between July and November 1976 in rodents. Serological tests show serum antibodies in rodents and are suggestive of suspected reservoirs. Ebola virus has been isolated from Asian Macaques (natural reservoirs of infection). They grow in cell cultures and guinea pigs.
4. Toga Viridae:
The name Toga viridae is derived from Latin toga, cloak, a reference to the envelope contained by the virus, and this family contains mainly alpha viruses.
Virology:
Toga viruses are spherical, enveloped and contain single stranded RNA in a core having cubic symmetry. Alpha viruses and pesti-viruses (60-70 nm diam.) are larger than Flavi viruses (30-50 nm diam.).
Pathogenesis of Toga Viruses:
Virus enters the body through the skin when infected insect vectors suck the blood. It multiplies in local lymph node and invades the blood into target organs (CNS in encephalitis, capillary endothelium in haemorrhagic fever, and liver in yellow fever).
Clinical Features of Toga Viruses:
Incubation period is 4-21 days. The infection is characterised by sudden onset with headache, nausea, vomiting, body ache, sometimes arthralgia. Subclinical infections are common; they may be severe. Table 62.3 shows the common arbo virus diseases in India.
Laboratory Diagnosis of Toga Viruses:
1. Isolation of virus:
The specimen of blood, CSF from acute disease is inoculated intra-cerebrally into suckling mice which later develop fatal encephalitis. These arbo viruses can be grown in tissue culture or in egg embryo and can be identified by haemagglutination inhibition test up to group. Neutralisation test can establish the species.
2. Serology:
Rising titre of haem-agglutinating and neutralizing antibodies can be demonstrated in the blood after a few days of onset of illness.
General Properties of Arbo Viruses:
1. Arbo viruses cause fatal encephalitis within 1 to 10 days after the intra-cerebral inoculation in 48 hour old suckling mice.
2. They have haemagglutinin for erythrocyte of newly hatched chicks and geese.
3. They multiply in continuous polypoid tissue culture at 37°C, but dengue and Ross River viruses multiply in continuous tissue cultures of Aedes albopictus mosquito cells.
4. Mosquito borne arbo viruses multiply in Aedes and Culex mosquitoes after blood sucking infected individuals.
5. Tick borne arbo viruses multiply in Ioxodid ticks.