Rift valley fever pathophysiology: Difference between revisions
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{{Rift valley fever}} | {{Rift valley fever}} | ||
{{CMG}}{{AE}} {{AAH}} | |||
==Overview== | |||
[[Rift valley fever|Rift valley fever]] is known to cause human infection by infecting the first line of defense in the body. The virus is able to survive and replicate inside [[Macrophage|macrophages]] and [[Dendritic cell|dendritic cells]] and release [[Interleukin 10|IL-10]] which further enhances the inflammation and spread of infection within the body. [[Hepatocyte|Liver cells]] are commonly infected by the virus which translated to right upper quadrant abdominal pain in the patient. | |||
==Pathophysiology== | |||
The pathophysiology of Rift valley fever mainly has three main stages: | |||
*'''Early infection''' : | |||
**The RVFV is an [[Arbovirus|arbovirus]], which means that it enters the human body during a mosquito bite. The [[Saliva|salivary]] content of the mosquito has properties amenable to the virus, which results in a higher load of virus to be transferred inside the human body. | |||
**Once inside the body, the virus is able to evade the first line of defense formed by the [[Macrophage|macrophages]] and [[Dendritic cell|dendritic cells]]. The virus possesses the ability to multiply inside macrophages. It also renders the macrophage incapable of releasing [[Cytokine|cytokines]] which would attract other [[White blood cells|white blood cells]] to eliminate the virus. <ref>McElroy AK, Nichol ST: Rift Valley fever virus inhibits a pro-inflammatory response in experimentally infected human monocyte derived macrophages and a pro-inflammatory cytokine response may be associated with patient survival during natural infection. Virology 2012;422:6-12</ref> | |||
**It is speculated that the virus uses macrophages and dendritic cells to increase its numbers by significant proportions. This is supported by the observation that the spread of the virus in animal models with no dendritic cells and macrophages is suppressed and slowed down by tremendous proportions. <ref>Gommet C, Billecocq A, Jouvion G, Hasan M, Zaverucha do Valle T, Guillemot L, Blanchet C, van Rooijen N, Montagutelli X, Bouloy M, Panthier JJ: Tissue tropism and target cells of NSs-deleted Rift Valley fever virus in live immunodeficient mice. PLoS Negl Trop Dis 2011;5:e1421.</ref> | |||
*'''Liver infection''' : | |||
**Regardless of the route of entry of the virus, it has the tendency to infect liver cells which is corroborated by the fact that [[Autopsy|postmortem]] examination of RVF cases show hepatic [[Inflammation|inflammation]] and injury. | |||
**Factors inducing [[Apoptosis|apoptosis]] are suppressed while those inhibiting apoptosis are increased when the virus infects liver cells. <ref>Jansen van Vuren P, Tiemessen CT, Paweska JT: Anti-nucleocapsid protein immune responses counteract pathogenic effects of Rift Valley fever virus infection in mice. PLoS One 2011;6:e25027.</ref> | |||
**It is postulated that the virus causes increased production of cytokines responsible for liver damage due to enhanced inflammatory response. IL-10 is one of the cytokines which are released in increased amounts during viral infection. | |||
**It is only when factors of adaptive immunity kick in, does the viral get cleared from the body. The removal and control [[Interleukin 10|IL-10]] and [[Interleukin 12|IL-12]] production form a key component of successful recovery. <ref>Dodd KA, McElroy AK, Jones ME, Nichol ST, Spiropoulou CF: Rift Valley fever virus clearance and protection from neurologic disease are dependent on CD4+ T cell and virus-specific antibody responses. J Virol 2013;87:6161-6171</ref> | |||
*'''Late Infection''' : | |||
**In cases where the virus persists in the body for longer periods of time, the virus is able to infect various types of neuronal cells. | |||
**It has been seen in animal models that [[Neuron|neurons]] present in the [[Olfaction|olfactory]] mucosa provide the virus with a potential entry point into the central nervous system. <ref>Smith DR, Steele KE, Shamblin J, Honko A, Johnson J, Reed C, Kennedy M, Chapman JL, Hensley LE: The pathogenesis of Rift Valley fever virus in the mouse model. Virology 2010;407:256-267.</ref> | |||
**Other studies have suggested that the virus also enters the [[Central nervous system|central nervous system]] through the [[Blood-brain barrier|blood-brain barrier]] and through layers protecting the [[Cerebrospinal fluid|CSF]]. | |||
**The anti-inflammatory factors in mosquito-saliva aid the virus cross the blood-brain barrier. Further clarification about viral invasion mechanisms will require more studies. | |||
==References== | ==References== | ||
Latest revision as of 14:06, 17 July 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aakash Hans, MD[2]
Overview
Rift valley fever is known to cause human infection by infecting the first line of defense in the body. The virus is able to survive and replicate inside macrophages and dendritic cells and release IL-10 which further enhances the inflammation and spread of infection within the body. Liver cells are commonly infected by the virus which translated to right upper quadrant abdominal pain in the patient.
Pathophysiology
The pathophysiology of Rift valley fever mainly has three main stages:
- Early infection :
- The RVFV is an arbovirus, which means that it enters the human body during a mosquito bite. The salivary content of the mosquito has properties amenable to the virus, which results in a higher load of virus to be transferred inside the human body.
- Once inside the body, the virus is able to evade the first line of defense formed by the macrophages and dendritic cells. The virus possesses the ability to multiply inside macrophages. It also renders the macrophage incapable of releasing cytokines which would attract other white blood cells to eliminate the virus. [1]
- It is speculated that the virus uses macrophages and dendritic cells to increase its numbers by significant proportions. This is supported by the observation that the spread of the virus in animal models with no dendritic cells and macrophages is suppressed and slowed down by tremendous proportions. [2]
- Liver infection :
- Regardless of the route of entry of the virus, it has the tendency to infect liver cells which is corroborated by the fact that postmortem examination of RVF cases show hepatic inflammation and injury.
- Factors inducing apoptosis are suppressed while those inhibiting apoptosis are increased when the virus infects liver cells. [3]
- It is postulated that the virus causes increased production of cytokines responsible for liver damage due to enhanced inflammatory response. IL-10 is one of the cytokines which are released in increased amounts during viral infection.
- It is only when factors of adaptive immunity kick in, does the viral get cleared from the body. The removal and control IL-10 and IL-12 production form a key component of successful recovery. [4]
- Late Infection :
- In cases where the virus persists in the body for longer periods of time, the virus is able to infect various types of neuronal cells.
- It has been seen in animal models that neurons present in the olfactory mucosa provide the virus with a potential entry point into the central nervous system. [5]
- Other studies have suggested that the virus also enters the central nervous system through the blood-brain barrier and through layers protecting the CSF.
- The anti-inflammatory factors in mosquito-saliva aid the virus cross the blood-brain barrier. Further clarification about viral invasion mechanisms will require more studies.
References
- ↑ McElroy AK, Nichol ST: Rift Valley fever virus inhibits a pro-inflammatory response in experimentally infected human monocyte derived macrophages and a pro-inflammatory cytokine response may be associated with patient survival during natural infection. Virology 2012;422:6-12
- ↑ Gommet C, Billecocq A, Jouvion G, Hasan M, Zaverucha do Valle T, Guillemot L, Blanchet C, van Rooijen N, Montagutelli X, Bouloy M, Panthier JJ: Tissue tropism and target cells of NSs-deleted Rift Valley fever virus in live immunodeficient mice. PLoS Negl Trop Dis 2011;5:e1421.
- ↑ Jansen van Vuren P, Tiemessen CT, Paweska JT: Anti-nucleocapsid protein immune responses counteract pathogenic effects of Rift Valley fever virus infection in mice. PLoS One 2011;6:e25027.
- ↑ Dodd KA, McElroy AK, Jones ME, Nichol ST, Spiropoulou CF: Rift Valley fever virus clearance and protection from neurologic disease are dependent on CD4+ T cell and virus-specific antibody responses. J Virol 2013;87:6161-6171
- ↑ Smith DR, Steele KE, Shamblin J, Honko A, Johnson J, Reed C, Kennedy M, Chapman JL, Hensley LE: The pathogenesis of Rift Valley fever virus in the mouse model. Virology 2010;407:256-267.