virus is part of the Semliki Forest SF group of Old World Alphaviruses. Predominantly New World viruses are associated with encephalitis, whereas poly-arthritis and a rash is predominantly associated with Old World alphaviruses. Although chikungunya virus is a member of the arthritogenic alphaviruses, there are also cases of meningoencephalitis and haemorrhagic disease.
RNA virus (see figure 1). Early 2006, the complete sequence of a chikungunya isolate from Reunion Island was made available through NCBI/ GenBank accession no. DQ443544.1. The virion consists of an envelope and a nucleocapsid. The chikungunya virus genome is 11,805 nucleotides long and encodes for two polyproteins – the non structural polyprotein consisting of four proteins (nsP1, nsP2, nsP3 and nsP4) and the structural polyprotein consisting of five proteins (Capsid, E3, E2, 6K and E1) (see figure 2). The 5’ end of the RNA molecule is capped with a 7-methylguanosine while the 3’ end is poly-adenylated. A subgenomic positive-strand RNA referred to as 26SRNA is transcribed from a negative-stranded RNA intermediate. This RNA serves as the mRNA for the synthesis of the viral structural proteins. Alphaviruses have conserved domains that play an important role in the regulation of viral RNA synthesis. These domains are found at the 5’ and 3’ ends as well as at the intergenic region. The E1 and E2 glycoproteins are expected to form heterodimers that associate as trimeric spikes on the viral surface covering the surface evenly. The envelope glycoproteins play a role in attachment to cells.Chikungunya Virus
Chikungunya is caused by the chikungunya virus (CHIKV), an arthropod-borne virus (arbovirus). Chikungunya is a member of the Alphavirus genus in the family Togaviridae. There are 29 different types of alphaviruses that cause diseases in humans and other mammals. These species of arboviruses have been classified into 7 antigenic complexes: Barmah Forest (BF), Eastern equine encephalitis (EEE), Middelburg (MID), Ndumu (NDU), Semliki Forest (SF), Venezuelan equine encephalitis (VEE), and Western equine encephalitis (WEE).
Alphaviruses can be divided into New World and Old World viruses. These two groups have evolved distinct ways of interacting with their respective hosts and differ in for instance their pathogenicity, and tropism. Chikungunya virus is part of the Semliki Forest SF group of Old World Alphaviruses. Predominantly New World viruses are associated with encephalitis, whereas poly-arthritis and a rash is predominantly associated with Old World alphaviruses. Although chikungunya virus is a member of the arthritogenic alphaviruses, there are also cases of meningoencephalitis and haemorrhagic disease.
The Alphavirus genus includes besides Chikungunya virus also Onyongnyong virus (ONNV) and Ross River virus (RRV). Chikungunya and Onyong nyong virus have 85% similarities in their genome. The Onyongnyong virus causes disease with symptoms very similar to chikungunya virus. It is also transmitted by mosquitos and the disease symptoms include arthritis, fever and rashes. This virus is so far limited to African countries mainly Uganda. It is not known to be fatal. The Ross River virus causes rashes and arthritis. This virus is epidemic in Australia and some of the surrounding islands. This virus is also transmitted by mosquitoes.
Chikungunya virus is a small (about 6070 nm-diameter), spherical, enveloped, positive-strand RNA virus (see figure 1). Early 2006, the complete sequence of a chikungunya isolate from Reunion Island was made available through NCBI/ GenBank accession no. DQ443544.1. The virion consists of an envelope and a nucleocapsid. The chikungunya virus genome is 11,805 nucleotides long and encodes for two polyproteins the non structural polyprotein consisting of four proteins (nsP1, nsP2, nsP3 and nsP4) and the structural polyprotein consisting of five proteins (Capsid, E3, E2, 6K and E1) (see figure 2). The 5 end of the RNA molecule is capped with a 7-methylguanosine while the 3 end is poly-adenylated. A subgenomic positive-strand RNA referred to as 26SRNA is transcribed from a negative-stranded RNA intermediate. This RNA serves as the mRNA for the synthesis of the viral structural proteins. Alphaviruses have conserved domains that play an important role in the regulation of viral RNA synthesis. These domains are found at the 5 and 3 ends as well as at the intergenic region. The E1 and E2 glycoproteins are expected to form heterodimers that associate as trimeric spikes on the viral surface covering the surface evenly. The envelope glycoproteins play a role in attachment to cells.
Virions located on the surface of the cell membrane enter the host cells by fusion and endocytosis of the viral envelope. The uncoating of the virions occurs in the cytoplasm. The site of mRNA transcription is in the cell cytoplasm. Replication is not restricted to a particular tissue or organ of the host so the virus replication occurs in various organs. The insect host initiates the virus replication. The genome replication is done in the cytoplasm (see figure 3).
History of Chikungunya
The disease was first was first detected in 1952 in Africa following an outbreak on the Makonde Plateau. This is a border area between Mozambique and Tanzania. The virus was isolated from the serum of a febrile patient from this area. The name chikungunya is derived from the Makonde word meaning that which bends up in reference to the stooped posture developed as a result of the arthritic symptoms of the disease. In Swahili this means the illness of the bended walker. Makonde is the language spoken by the Makonde, an ethnic group in southeast Tanzania and northern Mozambique.
According to the initial 1955 report about the epidemiology of the disease, the term chikungunya is derived from the Makonde root verb kungunyala, meaning to dry up or become contorted. The Makonde term was more specifically referred to as that which bends up. Subsequent authors apparently overlooked the references to the Makonde language and assumed that the term derived from Swahili, the lingua franca of the region. The erroneous attribution of the term as a Swahili word has been repeated in numerous print sources. Many other erroneous spellings and forms of the term are in common use including Chicken guinea, Chicken gunaya, and Chickengunya.
Chikungunya virus (CHIKV) likely originated in Central/East Africa, where the virus has been found to circulate in a sylvatic cycle between forest-dwelling mosquitoes and nonhuman primates. In these areas, sporadic human cases occur, but large human outbreaks were not common. However, in urban centers of Africa as well as throughout Asia, the virus can circulate between mosquitoes and naive human hosts in a cycle similar to that of dengue viruses.
Since its discovery in Africa, in 1952, chikungunya virus outbreaks have occurred occasionally, but recent outbreaks have spread the disease to other parts of the world. Numerous chikungunya re-emergences have been documented in Africa, Asia (India), and Europe, with irregular intervals of 220 years between outbreaks. Currently, chikungunya fever has been identified in nearly 40 countries. In 2008, chikungunya was listed as a US National Institute of Allergy and Infectious Diseases (NIAID) category C priority pathogen.
Chikungunya Signs Clinical Symptoms
The incubation period of chikungunya disease is from 2-6 days with symptoms usually appearing 47 d post-infection. If you have become infected with the chikungunya virus, you will noticed several symptoms some of which might include:
Rash
Pain in the Lower Back
Joint Pain (with or without the presence of swelling)
Vomiting
Nausea
Headaches
Chills
Fevers
Upon infection, chikungunya tends to present itself in two phases, the acute phase and the chronic phase:
Acute phase
The acute phase of chikungunya infection typically lasts from a few days to a couple of weeks. Characteristics of the acute phase include an abrupt onset of chills, fever reaching up to 40 C (104 F), vomiting, nausea, head ache, arthralgia (joint pain), and in some cases, maculopapular rash characterized by raised, spotted lesions. Severe joint and muscular pain is the main and the most problematic symptom of chikungunya. The pain is so intense that makes movement very difficult and prostrates its victims.
Typically, the fever lasts for two days and then ends abruptly. However, other symptoms like joint pain, intense headache, insomnia and an extreme degree of prostration, can last for about 5 to 7 days. During the acute phase, the viral load can reach 10E8 viral particles per ml of blood. The virus has been shown to infect epithelial and endothelial cells, primary fibroblasts and monocyte-derived macrophages, explaining the involvement of muscles, joints, and skin connective tissues.
Chronic phase
The chronic stage of chikungunya is characterized by poly-arthralgia that can last from weeks to years beyond the acute stage. Patients suffer from joint pains for up to 2 years, depending on their age. Ninety-five percent of infected adults are symptomatic after infection, and of these, most become disabled for weeks to months as a result of decreased dexterity, loss of mobility, and delayed reaction. Recurrent joint pain is experienced by 3040% of those infected. During early epidemics, rare but serious complications of the disease were noted, including myocarditis (inflammation of heart muscle), meningoencephalitis (inflammation of the brain and meninges), and mild haemorrhage. Other complications, such as uveitis and retinitis (inflammation of the eye), have been described.
Death caused by chikungunya infections appears to be rare. However, increases in crude death rates have been reported during the 20042008 epidemics.
More than half of patients who suffer from severe chikungunya fever are over 65 years old, and more than 33% of them die. Most of these adults have underlying medical conditions and appear to be more likely to suffer complications. Children are also disproportionately affected by severe chikungunya fever.
Pregnancy
During recent outbreaks, it was observed that most chikungunya infections occurring during pregnancy do not appear to result in transmission of the virus to the fetus. However, if the pregnant woman is viremic at the time of delivery, there is a risk for mother-to-child transmission with a vertical-transmission rate of almost fifty percent. Currently, there is no evidence that the virus is transmitted through breast milk.
Often symptoms in infected individuals are mild and most patients recover fully. Infection appears to confer life long immunity. Chikungunya virus infections are sometimes confused with dengue viral infection, because both diseases can present with high temperatures and myalgias (muscle pain) in people living in or returning from tropical areas (see figure 2, and also diagnosis of Dengue and Chikungunya).
Although these diseases share similar clinical features, prominent and prolonged joint pains are more consistent with chikungunya, whereas haemorrhage is more common in cases of dengue virus infection.
Source: CDC
