A member of the Togaviridae family of arthropod-born alphaviruses, the chikungunya virus (CHIKV) is spread by Aedes mosquito bites. Chikungunya fever, a rash, & arthralgia are the known signs of the virus. These are often preceded by potentially persistent and severe arthritic manifestations that can persist for months or even years.
Originally, CHIKV was primarily discovered in Asia and Africa after being first discovered in isolation in Tanzania’s Makonde Plateau in 1952. The phrase “which itself bends up” in Makonde is the source of the name Chikungunya. Reunion Island experienced the worst incidence, which affected roughly 35 percent of the population, between 2005 and 2006.
Since 2005, Chikungunya infections have primarily expanded in tropical & subtropical areas, finally making their way to the Americas in 2013 through the Caribbean Island of Saint Martin. Currently, CHIKV is pervasive throughout the world and has become a significant public health issue.
Epidemiology
The CHIKV virus was initially found in Tanzania around 1952, traveled to the Americas in 2013, and Florida in 2014, and then severely affected many Caribbean, South, and Central American nations. Even though the CHIKV infection is thought to be indigenous in some regions of West Africa, either human or vector movements have aided in its global spread.
Travelers carrying the virus bring it to new locations, whereby regional Aedes species start local spread. It has also been suggested that mosquitoes spread through the transportation of mosquito eggs and larvae via air and sea traffic. Although maternal-fetal & blood component transfer was also mentioned during most of the Reunion Island epidemics, a mosquito bite is the primary mode of transmission.
Additionally, Ae. albopictus and Ae. aegypti are the carriers of other well-known illnesses like Zika and Dengue, which can occasionally co-infect people. Differentiating diseases is now a problem because of the closeness in clinical manifestations and virtually the same geographical location.
Anatomy
Pathophysiology
The CHIKV virus is known to spread in two cycles: sylvan and urban. Africa is home to sylvatic infection, which involves an animal, a mosquito, and a human. The current outbreak in the Western World is primarily caused by urban transmissions, which occur when humans come into contact with mosquitoes. As previously indicated, Ae. aegypti served as the vector for the first transmission of CHIKV; however, the inclusion of Ae.
albopictus across an alteration in the E1 surface proteins boosted the virus’ fitness in this vector an its capacity to infect vertebrates. Upon inoculation & infection of individual epithelial & endothelium, fibroblasts, & monocyte-related macrophages, the CHIKV infection route begins. CHIKV moves through the circulatory and lymphatic systems, creating severe viremia after mounting an early immune reaction and hiding in the lymph glands.
It has been discovered that diseased monocyte-derived macrophages are responsible for the transportation of antigens into receptor sites (brain, muscles, liver, and joints). Acute symptoms are believed to be caused by an inflammatory response mediated by acute CD8+ and CD4+ T cells, as well as pro-inflammatory mediators, but chronic joint illness may be brought on by the permanent storage of infectious monocytes in the bones.
Etiology
Ae. albopictus and Aedes aegypti are the main vectors for the CHIKV virus (Asian) Tiger mosquito. Such mosquitoes possess biological traits that enable efficacious invasiveness, vectorial ability, and carrier competency, which set the stage for the spread of Chikungunya around the world. The species’ affinity for the bloodstream and its historical record of colonization outside of its own region underline its invasiveness.
The physiological traits of the species that permit transmission, also including viral consumption with blood feeding & subsequent infection of the mosquito’s saliva, determine the carrier competence. The most crucial component is vector capability, which defines epidemic potential but is primarily impacted by extrinsic (ecological problems) and intrinsic (barriers to mosquito infestation).
Vector competence variables that directly affect infectivity include vector density in relation to the host, the likelihood that the vector will feed on the host in a single day, viral survivability, as well as the extrinsic incubation time. Since Ae. aegypti has been present in the United States for even more than three hundred years, and Ae. albopictus has existed since 1985; the illness has the potential to spread globally due to its varied vector features.
Particularly, during the Indian Ocean pandemic in 2005 and 2006, it was shown that CHIKV has recently evolved to infect the urban arthropod vectors Ae. albopictus after acquiring a variation in its E1 cell membrane surface protein. Ae. albopictus and Ae. aegypti mosquitoes often constitute a concern to global health because of their specialized feeding on and connection with humans, as well as the mobility of both the host body and the vector.
Genetics
Prognostic Factors
Chikungunya infection is characterized by a significant post-chikungunya persistent polyarthralgia, which is described as joint symptoms last much longer than six weeks while having a low CFR (case fatality ratio).
According to a 2018 study on Aruba Chikungunya infections, post-CHIKV polyarthritis was present in 26 percent of all serology-diagnosed infected individuals.
Another 2018 study from French Guiana found that 40 percent & 31.3 percent, correspondingly, of all RT-PCR-proven subjects, had post-chikungunya musculoskeletal or rheumatic pain at three and six months.
A member of the Togaviridae family of arthropod-born alphaviruses, the chikungunya virus (CHIKV) is spread by Aedes mosquito bites. Chikungunya fever, a rash, & arthralgia are the known signs of the virus. These are often preceded by potentially persistent and severe arthritic manifestations that can persist for months or even years.
Originally, CHIKV was primarily discovered in Asia and Africa after being first discovered in isolation in Tanzania’s Makonde Plateau in 1952. The phrase “which itself bends up” in Makonde is the source of the name Chikungunya. Reunion Island experienced the worst incidence, which affected roughly 35 percent of the population, between 2005 and 2006.
Since 2005, Chikungunya infections have primarily expanded in tropical & subtropical areas, finally making their way to the Americas in 2013 through the Caribbean Island of Saint Martin. Currently, CHIKV is pervasive throughout the world and has become a significant public health issue.
The CHIKV virus was initially found in Tanzania around 1952, traveled to the Americas in 2013, and Florida in 2014, and then severely affected many Caribbean, South, and Central American nations. Even though the CHIKV infection is thought to be indigenous in some regions of West Africa, either human or vector movements have aided in its global spread.
Travelers carrying the virus bring it to new locations, whereby regional Aedes species start local spread. It has also been suggested that mosquitoes spread through the transportation of mosquito eggs and larvae via air and sea traffic. Although maternal-fetal & blood component transfer was also mentioned during most of the Reunion Island epidemics, a mosquito bite is the primary mode of transmission.
Additionally, Ae. albopictus and Ae. aegypti are the carriers of other well-known illnesses like Zika and Dengue, which can occasionally co-infect people. Differentiating diseases is now a problem because of the closeness in clinical manifestations and virtually the same geographical location.
The CHIKV virus is known to spread in two cycles: sylvan and urban. Africa is home to sylvatic infection, which involves an animal, a mosquito, and a human. The current outbreak in the Western World is primarily caused by urban transmissions, which occur when humans come into contact with mosquitoes. As previously indicated, Ae. aegypti served as the vector for the first transmission of CHIKV; however, the inclusion of Ae.
albopictus across an alteration in the E1 surface proteins boosted the virus’ fitness in this vector an its capacity to infect vertebrates. Upon inoculation & infection of individual epithelial & endothelium, fibroblasts, & monocyte-related macrophages, the CHIKV infection route begins. CHIKV moves through the circulatory and lymphatic systems, creating severe viremia after mounting an early immune reaction and hiding in the lymph glands.
It has been discovered that diseased monocyte-derived macrophages are responsible for the transportation of antigens into receptor sites (brain, muscles, liver, and joints). Acute symptoms are believed to be caused by an inflammatory response mediated by acute CD8+ and CD4+ T cells, as well as pro-inflammatory mediators, but chronic joint illness may be brought on by the permanent storage of infectious monocytes in the bones.
Ae. albopictus and Aedes aegypti are the main vectors for the CHIKV virus (Asian) Tiger mosquito. Such mosquitoes possess biological traits that enable efficacious invasiveness, vectorial ability, and carrier competency, which set the stage for the spread of Chikungunya around the world. The species’ affinity for the bloodstream and its historical record of colonization outside of its own region underline its invasiveness.
The physiological traits of the species that permit transmission, also including viral consumption with blood feeding & subsequent infection of the mosquito’s saliva, determine the carrier competence. The most crucial component is vector capability, which defines epidemic potential but is primarily impacted by extrinsic (ecological problems) and intrinsic (barriers to mosquito infestation).
Vector competence variables that directly affect infectivity include vector density in relation to the host, the likelihood that the vector will feed on the host in a single day, viral survivability, as well as the extrinsic incubation time. Since Ae. aegypti has been present in the United States for even more than three hundred years, and Ae. albopictus has existed since 1985; the illness has the potential to spread globally due to its varied vector features.
Particularly, during the Indian Ocean pandemic in 2005 and 2006, it was shown that CHIKV has recently evolved to infect the urban arthropod vectors Ae. albopictus after acquiring a variation in its E1 cell membrane surface protein. Ae. albopictus and Ae. aegypti mosquitoes often constitute a concern to global health because of their specialized feeding on and connection with humans, as well as the mobility of both the host body and the vector.
Chikungunya infection is characterized by a significant post-chikungunya persistent polyarthralgia, which is described as joint symptoms last much longer than six weeks while having a low CFR (case fatality ratio).
According to a 2018 study on Aruba Chikungunya infections, post-CHIKV polyarthritis was present in 26 percent of all serology-diagnosed infected individuals.
Another 2018 study from French Guiana found that 40 percent & 31.3 percent, correspondingly, of all RT-PCR-proven subjects, had post-chikungunya musculoskeletal or rheumatic pain at three and six months.
Awaiting FDA approval for chikungunya fever prophylaxis
https://www.ncbi.nlm.nih.gov/books/NBK534224/
medtigo
Chikungunya Virus Infection
Updated :
June 21, 2023
A member of the Togaviridae family of arthropod-born alphaviruses, the chikungunya virus (CHIKV) is spread by Aedes mosquito bites. Chikungunya fever, a rash, & arthralgia are the known signs of the virus. These are often preceded by potentially persistent and severe arthritic manifestations that can persist for months or even years.
Originally, CHIKV was primarily discovered in Asia and Africa after being first discovered in isolation in Tanzania’s Makonde Plateau in 1952. The phrase “which itself bends up” in Makonde is the source of the name Chikungunya. Reunion Island experienced the worst incidence, which affected roughly 35 percent of the population, between 2005 and 2006.
Since 2005, Chikungunya infections have primarily expanded in tropical & subtropical areas, finally making their way to the Americas in 2013 through the Caribbean Island of Saint Martin. Currently, CHIKV is pervasive throughout the world and has become a significant public health issue.
The CHIKV virus was initially found in Tanzania around 1952, traveled to the Americas in 2013, and Florida in 2014, and then severely affected many Caribbean, South, and Central American nations. Even though the CHIKV infection is thought to be indigenous in some regions of West Africa, either human or vector movements have aided in its global spread.
Travelers carrying the virus bring it to new locations, whereby regional Aedes species start local spread. It has also been suggested that mosquitoes spread through the transportation of mosquito eggs and larvae via air and sea traffic. Although maternal-fetal & blood component transfer was also mentioned during most of the Reunion Island epidemics, a mosquito bite is the primary mode of transmission.
Additionally, Ae. albopictus and Ae. aegypti are the carriers of other well-known illnesses like Zika and Dengue, which can occasionally co-infect people. Differentiating diseases is now a problem because of the closeness in clinical manifestations and virtually the same geographical location.
The CHIKV virus is known to spread in two cycles: sylvan and urban. Africa is home to sylvatic infection, which involves an animal, a mosquito, and a human. The current outbreak in the Western World is primarily caused by urban transmissions, which occur when humans come into contact with mosquitoes. As previously indicated, Ae. aegypti served as the vector for the first transmission of CHIKV; however, the inclusion of Ae.
albopictus across an alteration in the E1 surface proteins boosted the virus’ fitness in this vector an its capacity to infect vertebrates. Upon inoculation & infection of individual epithelial & endothelium, fibroblasts, & monocyte-related macrophages, the CHIKV infection route begins. CHIKV moves through the circulatory and lymphatic systems, creating severe viremia after mounting an early immune reaction and hiding in the lymph glands.
It has been discovered that diseased monocyte-derived macrophages are responsible for the transportation of antigens into receptor sites (brain, muscles, liver, and joints). Acute symptoms are believed to be caused by an inflammatory response mediated by acute CD8+ and CD4+ T cells, as well as pro-inflammatory mediators, but chronic joint illness may be brought on by the permanent storage of infectious monocytes in the bones.
Ae. albopictus and Aedes aegypti are the main vectors for the CHIKV virus (Asian) Tiger mosquito. Such mosquitoes possess biological traits that enable efficacious invasiveness, vectorial ability, and carrier competency, which set the stage for the spread of Chikungunya around the world. The species’ affinity for the bloodstream and its historical record of colonization outside of its own region underline its invasiveness.
The physiological traits of the species that permit transmission, also including viral consumption with blood feeding & subsequent infection of the mosquito’s saliva, determine the carrier competence. The most crucial component is vector capability, which defines epidemic potential but is primarily impacted by extrinsic (ecological problems) and intrinsic (barriers to mosquito infestation).
Vector competence variables that directly affect infectivity include vector density in relation to the host, the likelihood that the vector will feed on the host in a single day, viral survivability, as well as the extrinsic incubation time. Since Ae. aegypti has been present in the United States for even more than three hundred years, and Ae. albopictus has existed since 1985; the illness has the potential to spread globally due to its varied vector features.
Particularly, during the Indian Ocean pandemic in 2005 and 2006, it was shown that CHIKV has recently evolved to infect the urban arthropod vectors Ae. albopictus after acquiring a variation in its E1 cell membrane surface protein. Ae. albopictus and Ae. aegypti mosquitoes often constitute a concern to global health because of their specialized feeding on and connection with humans, as well as the mobility of both the host body and the vector.
Chikungunya infection is characterized by a significant post-chikungunya persistent polyarthralgia, which is described as joint symptoms last much longer than six weeks while having a low CFR (case fatality ratio).
According to a 2018 study on Aruba Chikungunya infections, post-CHIKV polyarthritis was present in 26 percent of all serology-diagnosed infected individuals.
Another 2018 study from French Guiana found that 40 percent & 31.3 percent, correspondingly, of all RT-PCR-proven subjects, had post-chikungunya musculoskeletal or rheumatic pain at three and six months.
https://www.ncbi.nlm.nih.gov/books/NBK534224/
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