A single-stranded RNA virus with an envelope, the West Nile virus belongs to the Flaviviridae family. It is an arbovirus that infects individuals after a mosquito bite. It is well-documented to cause disease in people with a variety of symptoms.
However, most West Nile virus carriers exhibit no symptoms. A viral illness with fever affects about 1 in 4 individuals, while neuroinvasive disease strikes about 1 in 200.
Epidemiology
The West Nile virus was initially detected in Uganda in 1937. It returned in 1999, with records of seven fatalities and 62 cases of encephalitis in New York; this was the virus’s first appearance in the western hemisphere. The West Nile virus is currently found in Africa, Asia, Europe, North America, the Middle East, and Australia.
The virus’s initial outbreaks were mainly self-limited and mild symptoms. West Nile virus was linked to severe neurologic illness in the mid-1990s. Encephalitis and meningitis were found in less than 1% of infected patients, with a 10% fatality rate, according to a comprehensive literature analysis from 2013. 25% of those infected have West Nile fever, while the remaining 75% exhibit minimal to no symptoms.
Due to this characteristic, viral infections are vastly underreported. The life cycle of the mosquito vector and the amplification from the bird-mosquito-bird cycle, outbreaks frequently occur in the late summer and early fall. In warmer regions, incidents might occur yearly.
Anatomy
Pathophysiology
When the mosquito bites, it ingests the host’s saliva while spreading the virus. Viral replication in keratinocytes and dermal dendritic cells occurs immediately after transmission. The subsequent phase, known as the visceral-organ distribution phase, involves the transmission of the virus to the visceral organs and viral replication in draining lymph nodes and viremia. The central nervous system is affected by the third and final phases.
Uncertainty encompasses how viruses enter the central nervous system; however, it may involve direct axonal retrograde transport, passive endothelial transport, and infected macrophages passing through the blood-brain barrier. The virus predominantly causes inflammation once it enters the central nervous system, which leads to a loss of neurons in the gray matter of the brainstem and spinal cord.
Etiology
Humans contract the West Nile virus after being bitten by a mosquito. The most prevalent vector is a mosquito known as Culex. In addition to humans, the West Nile virus can infect numerous other creatures, including birds, horses, and dogs. The most suitable hosts for containing and promoting viral proliferation may be wild birds.
Because of the minimal and temporary viral levels in the bloodstream, humans are regarded as unintentional hosts. Infected donor blood, breast milk, organs, or transplacental infection are further, albeit uncommon, transmission routes.
One percent of persons will experience severe symptoms, and those over 50 have higher morbidities overall. Neurological problems are frequent. Unfortunately, a lack of federal financing has made it difficult for many states to maintain active surveillance of this virus.
Genetics
Prognostic Factors
For most patients, the prognosis is favorable. The majority of affected people show no symptoms. Few individuals’ viral syndrome symptoms last up to 10 days. However, in neuroinvasive illness, the least common but most severe clinical presentation has a death rate of around 10%.
The risk of neuroinvasive WNV is highest in the elderly population. A wide range of neurologic impairments is present, which may last for years or even become irreversible.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK544246/
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A single-stranded RNA virus with an envelope, the West Nile virus belongs to the Flaviviridae family. It is an arbovirus that infects individuals after a mosquito bite. It is well-documented to cause disease in people with a variety of symptoms.
However, most West Nile virus carriers exhibit no symptoms. A viral illness with fever affects about 1 in 4 individuals, while neuroinvasive disease strikes about 1 in 200.
The West Nile virus was initially detected in Uganda in 1937. It returned in 1999, with records of seven fatalities and 62 cases of encephalitis in New York; this was the virus’s first appearance in the western hemisphere. The West Nile virus is currently found in Africa, Asia, Europe, North America, the Middle East, and Australia.
The virus’s initial outbreaks were mainly self-limited and mild symptoms. West Nile virus was linked to severe neurologic illness in the mid-1990s. Encephalitis and meningitis were found in less than 1% of infected patients, with a 10% fatality rate, according to a comprehensive literature analysis from 2013. 25% of those infected have West Nile fever, while the remaining 75% exhibit minimal to no symptoms.
Due to this characteristic, viral infections are vastly underreported. The life cycle of the mosquito vector and the amplification from the bird-mosquito-bird cycle, outbreaks frequently occur in the late summer and early fall. In warmer regions, incidents might occur yearly.
When the mosquito bites, it ingests the host’s saliva while spreading the virus. Viral replication in keratinocytes and dermal dendritic cells occurs immediately after transmission. The subsequent phase, known as the visceral-organ distribution phase, involves the transmission of the virus to the visceral organs and viral replication in draining lymph nodes and viremia. The central nervous system is affected by the third and final phases.
Uncertainty encompasses how viruses enter the central nervous system; however, it may involve direct axonal retrograde transport, passive endothelial transport, and infected macrophages passing through the blood-brain barrier. The virus predominantly causes inflammation once it enters the central nervous system, which leads to a loss of neurons in the gray matter of the brainstem and spinal cord.
Humans contract the West Nile virus after being bitten by a mosquito. The most prevalent vector is a mosquito known as Culex. In addition to humans, the West Nile virus can infect numerous other creatures, including birds, horses, and dogs. The most suitable hosts for containing and promoting viral proliferation may be wild birds.
Because of the minimal and temporary viral levels in the bloodstream, humans are regarded as unintentional hosts. Infected donor blood, breast milk, organs, or transplacental infection are further, albeit uncommon, transmission routes.
One percent of persons will experience severe symptoms, and those over 50 have higher morbidities overall. Neurological problems are frequent. Unfortunately, a lack of federal financing has made it difficult for many states to maintain active surveillance of this virus.
For most patients, the prognosis is favorable. The majority of affected people show no symptoms. Few individuals’ viral syndrome symptoms last up to 10 days. However, in neuroinvasive illness, the least common but most severe clinical presentation has a death rate of around 10%.
The risk of neuroinvasive WNV is highest in the elderly population. A wide range of neurologic impairments is present, which may last for years or even become irreversible.
https://www.ncbi.nlm.nih.gov/books/NBK544246/
medtigo
West Nile Virus (WNV) Infection
Updated :
November 18, 2022
A single-stranded RNA virus with an envelope, the West Nile virus belongs to the Flaviviridae family. It is an arbovirus that infects individuals after a mosquito bite. It is well-documented to cause disease in people with a variety of symptoms.
However, most West Nile virus carriers exhibit no symptoms. A viral illness with fever affects about 1 in 4 individuals, while neuroinvasive disease strikes about 1 in 200.
The West Nile virus was initially detected in Uganda in 1937. It returned in 1999, with records of seven fatalities and 62 cases of encephalitis in New York; this was the virus’s first appearance in the western hemisphere. The West Nile virus is currently found in Africa, Asia, Europe, North America, the Middle East, and Australia.
The virus’s initial outbreaks were mainly self-limited and mild symptoms. West Nile virus was linked to severe neurologic illness in the mid-1990s. Encephalitis and meningitis were found in less than 1% of infected patients, with a 10% fatality rate, according to a comprehensive literature analysis from 2013. 25% of those infected have West Nile fever, while the remaining 75% exhibit minimal to no symptoms.
Due to this characteristic, viral infections are vastly underreported. The life cycle of the mosquito vector and the amplification from the bird-mosquito-bird cycle, outbreaks frequently occur in the late summer and early fall. In warmer regions, incidents might occur yearly.
When the mosquito bites, it ingests the host’s saliva while spreading the virus. Viral replication in keratinocytes and dermal dendritic cells occurs immediately after transmission. The subsequent phase, known as the visceral-organ distribution phase, involves the transmission of the virus to the visceral organs and viral replication in draining lymph nodes and viremia. The central nervous system is affected by the third and final phases.
Uncertainty encompasses how viruses enter the central nervous system; however, it may involve direct axonal retrograde transport, passive endothelial transport, and infected macrophages passing through the blood-brain barrier. The virus predominantly causes inflammation once it enters the central nervous system, which leads to a loss of neurons in the gray matter of the brainstem and spinal cord.
Humans contract the West Nile virus after being bitten by a mosquito. The most prevalent vector is a mosquito known as Culex. In addition to humans, the West Nile virus can infect numerous other creatures, including birds, horses, and dogs. The most suitable hosts for containing and promoting viral proliferation may be wild birds.
Because of the minimal and temporary viral levels in the bloodstream, humans are regarded as unintentional hosts. Infected donor blood, breast milk, organs, or transplacental infection are further, albeit uncommon, transmission routes.
One percent of persons will experience severe symptoms, and those over 50 have higher morbidities overall. Neurological problems are frequent. Unfortunately, a lack of federal financing has made it difficult for many states to maintain active surveillance of this virus.
For most patients, the prognosis is favorable. The majority of affected people show no symptoms. Few individuals’ viral syndrome symptoms last up to 10 days. However, in neuroinvasive illness, the least common but most severe clinical presentation has a death rate of around 10%.
The risk of neuroinvasive WNV is highest in the elderly population. A wide range of neurologic impairments is present, which may last for years or even become irreversible.
https://www.ncbi.nlm.nih.gov/books/NBK544246/
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