INTRODUCTION:
The Chandipura Virus (CHPV) is one of the most recent and underdiagnosed classes of deadly viruses. Originally an arthropod-borne virus (Arbovirus), CHPV (Fig. 1) is a vesiculo virus belonging to the Rhabdoviridae family that is unique to India.1 It was discovered in 1966 at the Virus Research Centre (VRC) in Pune by Bhatt and Rodriguez. The Chandipura virus was called when it was unintentionally discovered while examining patients with fever in Chandipura village, northern Maharashtra, close to Nagpur district, for dengue or chikungunya viral etiology.2
As an arbovirus, CHPV is a member of a class of viruses with different taxonomies that are spread by the same mechanism across vertebrate hosts. Many viruses that infect arthropods are Togavirideae (Alpha viruses), Flaviviridae, Bunyaviradeae, and Rehoviradeae are the families of arboviruses. Usually, mosquitoes, ticks, sand flies, or less frequently, other insects, are the arthropods that spread these viruses. According to Peiris et al. (2008), the manifestation of CHPV begins as an influenza-like sickness that is accompanied by vomiting, altered awareness, decreased neurological functioning, and stomach discomfort3. It results in encephalitis, which is a localized or diffuse inflammatory disorder of the brain parenchyma linked to neurological problems. The two main kinds of encephalitis pathophysiology are: auto-immune mediated encephalitis and infection-related encephalitis.3 Whereas auto-immune mediated encephalitis is linked to systemic infection or vaccination and is mediated by a pathologic immune response primarily directed against myelin, affecting the brain and spinal cord, infection-related encephalitis is a direct result of viral entry into the central nervous system. Since there is no particular therapy for arbovirus-borne illnesses, they are managed symptomatically.4
Epidemiology: India-specific:
A 2003 study by NIV scientists brought CHPV to the public's attention. During a widespread epidemic of a severe neurological disease in young children with a high case-fatality rate, encephalitis was identified as the underlying cause and was allegedly linked to viral infection.5,6 Seizures, diarrhea, vomiting, fever with an abrupt start, and impaired sensory perception were the main symptoms of the sickness. Death or recovery happened quickly between two and three days and survivors did not experience any aftereffects. Due in part to the absence of cell growth in the CSF, these results led to the clinical diagnosis of "brainstem encephalitis," whose cause was identified as CHPV.7
The validity of the findings linking CHPV to the pathophysiology of pandemic encephalopathy has been questioned by certain specialists.8 Large outbreaks of viral encephalitis have been linked to the Chandipura Virus, a commonly known rhabdovirus, according to a CDC arbovirus researcher. Nonetheless, strong evidence points to a "questionable" link between the virus and the sickness.9 The comprehensive neurological results were considered to show that the epidemic was an immediate catastrophic brain catastrophe rather than "encephalitis." The lesion location was identified as the middle cerebral artery's brain supply area. Although the specifics of the artery pathology were not examined, it was hypothesized that the cause was vasculitis-related spasm or temporary blockage rather than thromboembolism.5,6 It was fresh knowledge that there may be a "acute brain attack." Inflammatory lesions in histology or pathogen invasion were not shown clinically. According to Rao et al. (2004a, b); Ismail (2004), if the CHPV etiology is accurate, vasculitis rather than encephalitis would be the disease's mediator. Interesting findings have been obtained from yet another study on acute encephalitis in Andhra Pradesh.5,6,10 In a hospital From May 2005 to April 2006, every child case of encephalitis in Hyderabad was prospectively studied. Out of the 90 patients, 25 had CHPV infection evidence detected by PCR, IgM antibody, or seroconversion. The virus was not, however, isolated. 91–73% of contacts of patients under the age of 15 and 94–97% of contacts of cases above the age of 15 exhibited antibody evidence of prior CHPV infection.11
Figure 1: Chandipura Virus (CHPV) seen by transmission electron microscopy.12
Transmission:
P. argentipes is one of the common species in various CHPV-endemic locations of India. According to research, 65 percent of P. argentipes were oral CHPV sensitive. Because of this species' issues with refeeding, transmission tests were conducted via intra-thoracic injection. Mice were effectively infected with CHPV during a 24-hour incubation period. Within the infected flies, a minimum estimated transmission rate of 32% was observed. Using the reverse transcription–polymerase chain reaction and immunofluorescent antibody test, CHPV was found and verified in both mice and sand flies. Regarding the epidemiology of CHPV, P. argentipes's sensitivity to the virus and its ability to spread it through bites are significant. To ascertain if men may play a part in preserving or sustaining CHPV activity in nature, comparable lab studies were carried out on Phlebotomus papatasi. According to this study, male infected sand flies have the ability to transmit the virus to female flies during mating. When uninfected females mated with sick males, the infection rate was found to be 12.5%. In the natural cycle of CHPV, the incidence of venereal transmission of this virus may be epidemiologically significant.13
Figure 2. shows the Indian region affected by the Chandipura outbreak.
Figure 3: The total number of cases of Chandipura illness and encephalitis in different Indian states
Etiology:
It is thought that the Chandipura virus is zoonotic, which means that it spreads from animal populations to human populations. Infections in humans can result from direct or indirect contact with ticks, mosquitoes, and sandflies. It is still necessary to conduct research and monitoring since the precise animal reservoirs and ways of transmission are still being uncovered.
The virus replicates in the central nervous system (CNS) by producing vireamia and bridging the blood-brain barrier. Virus-specific IgM antibodies successfully stop the virus from spreading, but the virus keeps replicating in the central nervous system. The virus primarily impacts immunity by significantly boosting the release of pro-inflammatory cytokines. Additionally, it significantly lowers CD4, CD8, and CD19 cell counts. Moreover, cytokines make the blood-brain barrier more permeable, which facilitates viral entry into the central nervous system (CNS). Viral replication in the CNS is what causes neurological disorders and death.14
Virology:
Virus life cycle:
The vesiculovirus life cycle may be broken down into two distinct stages:
1. Viral particle adsorption and cell penetration.
2. Core RNP is released from late endosomal vesicles and uncoated, entering the cytosol.
3. Viral polymerase's transcription of the genome.
4. Viral messenger RNA translation.
5. Viral protein post-translational changes.
6. The viral genome is replicated.
7. Progeny particle assembly and ultimately the blossoming of mature virion.
A vesiculovirus's whole life cycle is cytosolic within an infected cell.15 In order to create five monocistronic capped and polyadenylated viral mRNAs as well as short leader RNA, successive transcription starting at the 3′ end of the genome uses the genome RNA encased in nucleocapsid protein N as a template. Large protein L, the catalytic component of viral RNA-dependent RNA polymerase (RdRp), and phosphorylated version of protein P, which functions as a transcriptional activator, make up RdRp. Viral polypeptides accumulate in infected cells as a result of viral mRNA translation, which also sets the ground for the start of genome replication.15,16 In order to duplicate a whole genomic template into a precise polycistronic complement that serves as a replication intermediate to create many more copies of (−) ve sense genomes during subsequent rounds of replication, the same polymerase changes to replicative mode. Secondary transcription occurs when transcription occurs in progeny (−) ve sense genomes. Notably, N consistently keeps virus-specific genomic analogues encapsidated rather than mRNAs, and it is thought that the nascent genome gradually encapsidates over time. According to Banerjee (1987a) and Barr et al. (2002), RNA is required for replication and/or for shielding the replication product from cellular RNases. The many parts of CHPV and their function in the viral life cycle will be covered here.15,16
Diagnosis:
Similar to the flu, the chandipura virus produces fever and acute encephalitis, or inflammation of the brain. The virus belongs to the Rhabdoviridae family's Vesiculovirus genus. The main vectors of transmission include sandflies, ticks, and mosquitoes. In Andhra Pradesh and Gujarat, where the epidemics occurred in 2003–2004, case mortality rates ranged from 56-75%, with classic encephalitic signs.
A Chandipura virus infection might cause anything from minor respiratory discomfort to more serious problems.
Common symptoms:
· Fever
· Fatigue
· Vomiting
· Convulsions17
The overall diagnosis is established along the same lines as encephalitis; a computed tomography scan (CT scan) of a kid infected with CHPV. The ventricles exhibit aberrant dilatation on the right side of the brain (orange area) (Whitley and Gann, 2002). Previous research has demonstrated the value of real-time PCR as an indication of the degree of current infection as well as its efficacy in detecting and quantifying viral load. At the moment, CHPV quantification is carried out in vitro (cell lines), in vivo (mice), and in ovo (eggs), with the 50% endpoint approach being used to calculate the viral titer. Given the high fatality rate and rapidity of the illness, nested RT-PCR for viral RNA identification is the preferred diagnostic technique. possess IgM antibodies against CHPV. As an effective substitute, real-time one-step RT-PCR assays provide a number of benefits, including high sensitivity, speed, precision, and repeatability.18
Treatment and preventive measure:17
The Chandipura virus (CHPV) is a potentially lethal illness that spreads quickly and primarily affects youngsters. As of right now, supportive care is the mainstay of CHPV management as there is no particular antiviral medication available.
Supportive Care:
Handling Symptoms
1. Pain and fever reduction: Acetaminophen and other antipyretics are effective in lowering temperature and relieving pain.
2. Hydration: To avoid dehydration, it is essential to make sure patients are getting enough fluids, particularly if they are vomiting and have a high temperature.
3. Control of Seizures: Anticonvulsant drugs may be used to treat seizures, which are frequently seen in severe CHPV infections.
Neurological Treatment:
1. Monitoring: In order to identify any worsening of symptoms, it is imperative to continuously assess neurological condition.
2. Intensive treatment Unit (ICU) Admission: In severe cases of encephalitis or coma, patients may need to be kept under careful observation and receive supportive treatment, which may include mechanical ventilation if needed.
Best Treatment for Chandipura Virus Prevention
Treatment and their description
1. Antiviral medication: Use prescribed antiviral drugs to manage symptoms and reduce virus spread
2. Hydration: Ensure adequate fluid intake to prevent dehydration
3. Pain relief: Use analgesics like acetaminophen to relieve pain and fever
4. Rest: Get plenty of rest to support the immune system.
5. Immunoglobulin therapy: Administer immune globulins if recommended by a healthcare provider.
6. Fever management: Use tepid sponging and antipyretics to control fever.
7. Nutrition: Maintain a balanced diet to support overall health.
8. Isolation: Isolate infected individuals to prevent virus transmission.
9. Symptomatic treatment: Address specific symptoms like nausea and vomiting as they arise.
10. Regular monitoring: Monitor vital signs and symptoms regularly to manage health effectively.
Preventive measure:
Vector Control Measures:
1. Regular use of pesticides within and around houses can effectively lower the number of sandflies. In rural and semi-rural locations where sandflies are more prevalent, this is particularly crucial.
2. Larvicidal Treatments: Sandfly larvae can be controlled before they become adults by applying larvicides to possible breeding locations, such as damp soil and stagnant water.
3. Environmental Management: Sandflies' populations can be decreased by removing plants, trash, and other detritus from the vicinity of habitations.
Personal Protective Measures:
1. Use insect repellents on exposed skin and clothes that include DEET, picaridin, or other potent chemicals. These insect repellents can lessen the chance of getting bitten by sandflies.
2. Wear long sleeves, long trousers, socks, and closed shoes as protective clothing, especially in the early morning and late evening when sandflies are most active.
3. Bed Nets: To avoid getting bit by sandflies while you sleep, use bed nets coated with pesticides. To ensure total protection, make sure the nets are securely tucked under the mattress.
4. Window Screens: To keep sandflies out of residential areas, install fine mesh screens on windows and doors.
10 Best Tips for Chandipura Virus Prevention
Preventive tips and their description:
1. Use insect repellent: Apply repellent to exposed skin to avoid mosquito bites.
2. Wear protective clothing: Use long sleeves and pants to reduce skin exposure.
3. Use mosquito nets: Sleep under insecticide-treated nets to prevent mosquito bites.
4. Eliminate stagnant water:- Remove standing water where mosquitoes breed.
5. Install window screens: Use screens on windows and doors to keep mosquitoes out.
6. Maintain clean surroundings: Keep the environment clean to reduce mosquito habitats.
7. Use mosquito coils or vaporizers: Use coils or electric vaporizers to repel mosquitoes indoors.
8. Community awareness: Educate the community about preventive measures and symptoms.
9. Monitor symptoms: Seek medical attention if symptoms of the virus appear.
10. Support vector control programs: Participate in local mosquito control and eradication efforts.
Research and Future Directions:
1. Antiviral Development:
1. Research: To find possible antiviral drugs that might be helpful against CHPV, scientists are doing active research.
2. Clinical studies: To evaluate the safety and effectiveness of experimental therapies in treating CHPV, clinical studies may be conducted.
2. Vaccine Development:
1. Research is still being done to create a CHPV vaccine, which may offer long-term defense against the infection.
2. Difficulties: Creating a vaccination requires overcoming difficulties including making sure it is safe and effective for the intended audience, which is mostly youngsters.
CONCLUSION:
Periodically, there seems to be an outbreak of CHPV infection in the population starting around age 15. Nevertheless, there have been eerily few documented cases of acute brain sickness that are purportedly brought on by it.
It's a vesiculovirus, and a lot of information regarding this genus's host-virus research is available. Nonetheless, because CHPV is a common agent of infection in a number of host species in India, fundamental research on the virus must continue, and its biology must be understood to the fullest extent feasible. We have gone over its life cycle, genesis, target population, and our attempts to control, manage, and eradicate it. It is crucial to increase surveillance in places like tropical nations to estimate the illness burden of CHPV very needful and vital
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Received on 30.08.2024 Revised on 09.10.2024 Accepted on 08.11.2024 Published on 17.12.2024 Available online on December 23, 2024 Asian Journal of Pharmaceutical Research. 2024; 14(4):392-396. DOI: 10.52711/2231-5691.2024.00062 ©Asian Pharma Press All Right Reserved
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