Poliovirus: Difference between revisions

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== Metabolic effects ==
== Metabolic effects ==
A study of poliovirus found that polio infection rapidly decreases (45% decrease) cellular oxygen consumption (and thus energy production through [[cellular respiration]]) by inhibiting [[succinate dehydrogenase]] (55% decrease in activity) and blocking mitochondrial electron transport at or between complexes I and III.<ref>{{Cite journal|last=Koundouris|first=A|date=May 2000|title=Poliovirus Induces an Early Impairment of Mitochondrial Function by Inhibiting Succinate Dehydrogenase Activity|url=https://www.ncbi.nlm.nih.gov/pubmed/10814509|journal=Biochemical and Biophysical Research Communications|volume=271|pages=610-4|via=}}</ref>
A study of poliovirus found that polio infection rapidly decreases (45% decrease) cellular oxygen consumption (and thus energy production through [[cellular respiration]]) by inhibiting [[succinate dehydrogenase]] (55% decrease in activity) and blocking mitochondrial electron transport at or between complexes I and III.<ref>{{Cite journal | last = Koundouris | first=A | date = May 2000| title = Poliovirus Induces an Early Impairment of Mitochondrial Function by Inhibiting Succinate Dehydrogenase Activity|url=https://www.ncbi.nlm.nih.gov/pubmed/10814509|journal=Biochemical and Biophysical Research Communications|volume=271 | pages = 610-4|via=}}</ref>


== Relationship to myalgic encephalomyelitis ==
== Relationship to myalgic encephalomyelitis ==
Prior to the poliovirus vaccine, several [[List of myalgic encephalomyelitis and chronic fatigue syndrome outbreaks|outbreaks]] of what later came to be called [[myalgic encephalomyelitis]] coincided with confirmed outbreaks of [[poliomyelitis]]  including the [[1934 Los Angeles atypical polio outbreak|1934 Los Angeles outbreak]], the [[1948-49 Akureyri outbreak|1948 Akureyri, Iceland outbreak]], and 1949 outbreak in [[1949-53 Adelaide outbreak|Adelaide, Australia]]. Many outbreaks were initially misinterpreted as clusters of [[poliomyelitis]] or [[abortive poliomyelitis]], hence one of [[myalgic encephalomyelitis|ME]]'s earliest names, [[atypical polio]]. It is not known whether there is a direct relationship between polio outbreaks and ME or if outbreaks of ME were more likely to be reported when public health authorities were already mobilized for an earlier crisis.
Prior to the poliovirus vaccine, several [[List of myalgic encephalomyelitis and chronic fatigue syndrome outbreaks|outbreaks]] of what later came to be called [[myalgic encephalomyelitis]] coincided with confirmed outbreaks of [[poliomyelitis]]  including the [[1934 Los Angeles atypical polio outbreak|1934 Los Angeles outbreak]], the [[1948-49 Akureyri outbreak|1948 Akureyri, Iceland outbreak]], and 1949 outbreak in [[1949-53 Adelaide outbreak|Adelaide, Australia]]. Many outbreaks were initially misinterpreted as clusters of [[poliomyelitis]] or [[abortive poliomyelitis]], hence one of [[myalgic encephalomyelitis|ME]]'s earliest names, [[atypical polio]]. It is not known whether there is a direct relationship between polio outbreaks and ME or if outbreaks of ME were more likely to be reported when public health authorities were already mobilized for an earlier crisis.


No serological evidence of polio was ever found in these outbreaks and the ultimate pattern of the outbreaks differed in significant ways, chief among them, the tendency to affect adults rather than children, and to result in higher [[morbidity]] than poliomyelitis but no [[mortality]].<ref name=":02">{{Cite journal|last=Parish|first=JG|date=1978|title=Early outbreaks of 'epidemic neuromyasthenia'|url=https://www.ncbi.nlm.nih.gov/pubmed/370810|journal=Postgraduate Medical Journal|volume=54|pages=711-7|via=}}</ref> Findings in several outbreaks seemed to suggest that symptoms were caused by an [[enterovirus]] distinct from but related to polio including findings of mild, diffuse [[peripheral nervous system]] damage in monkeys infected with the virus; a stronger response to polio vaccination in children who had been in epidemic areas; and seasonal patterns of infection resembling polio.<ref name=":02" />
No serological evidence of polio was ever found in these outbreaks and the ultimate pattern of the outbreaks differed in significant ways, chief among them, the tendency to affect adults rather than children, and to result in higher [[morbidity]] than poliomyelitis but no [[mortality]].<ref name=":02">{{Cite journal | last = Parish | first = JG | date = 1978| title = Early outbreaks of 'epidemic neuromyasthenia'|url=https://www.ncbi.nlm.nih.gov/pubmed/370810|journal=Postgraduate Medical Journal|volume=54 | pages = 711-7|via=}}</ref> Findings in several outbreaks seemed to suggest that symptoms were caused by an [[enterovirus]] distinct from but related to polio including findings of mild, diffuse [[peripheral nervous system]] damage in monkeys infected with the virus; a stronger response to polio vaccination in children who had been in epidemic areas; and seasonal patterns of infection resembling polio.<ref name=":02" />
== Cross-immunity ==
== Cross-immunity ==
It is theorized that exposure to one enterovirus may confer partial immunity or improved immune response to another enteroviruses. One study compared schoolchildren in [[Estonia]], who were inoculated with the Sabin, live attenuated virus polio vaccine, to [[Finland|Finnish]] schoolchildren, who were inoculated with the Salk, inactivated vaccine.<ref>{{Cite journal|last=Juhela|first=S|date=July 1999|title=Comparison of enterovirus-specific cellular immunity in two populations of young children vaccinated with inactivated or live poliovirus vaccines|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905481/|journal=Clinical & Experimental Immunology|volume=117|pages=100–105|via=}}</ref> Estonian children had stronger [[T cell]] responses to [[coxsackievirus B4]] and poliovirus type 1, and stronger expression of [[IFN-γ]] when exposed to poliovirus challenge as compared to Finnish children. Finnish children have weaker cellular immunity against enteroviruses at the age of 9 months compared with Estonian children at the same age. (Finland has a rate of [[diabetes#Type_1|type 1 diabetes]] three times the rate of Estonia. Coxsackie B4 has been associated with Type 1 diabetes.) An unintended consequence of widespread polio vaccination may have been impaired immunity to other enteroviruses, such as [[Coxsackievirus|Coxsackie]] and [[echoviruses]].   
It is theorized that exposure to one enterovirus may confer partial immunity or improved immune response to another enteroviruses. One study compared schoolchildren in [[Estonia]], who were inoculated with the Sabin, live attenuated virus polio vaccine, to [[Finland|Finnish]] schoolchildren, who were inoculated with the Salk, inactivated vaccine.<ref>{{Cite journal | last= Juhela | first = S | date = July 1999| title = Comparison of enterovirus-specific cellular immunity in two populations of young children vaccinated with inactivated or live poliovirus vaccines|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905481/|journal=Clinical & Experimental Immunology|volume=117|pages=100–105|via=}}</ref> Estonian children had stronger [[T cell]] responses to [[coxsackievirus B4]] and poliovirus type 1, and stronger expression of [[IFN-γ]] when exposed to poliovirus challenge as compared to Finnish children. Finnish children have weaker cellular immunity against enteroviruses at the age of 9 months compared with Estonian children at the same age. (Finland has a rate of [[diabetes#Type_1|type 1 diabetes]] three times the rate of Estonia. Coxsackie B4 has been associated with Type 1 diabetes.) An unintended consequence of widespread polio vaccination may have been impaired immunity to other enteroviruses, such as [[Coxsackievirus|Coxsackie]] and [[echoviruses]].   


There is indirect evidence of cross-immunity between [[poliovirus]] and the unidentified virus or viruses in epidemic myalgic encephalomyelitis outbreaks. After the 1948-1949 [[1948-49 Akureyri outbreak|Akureyri outbreak]] in Iceland, children in areas that had been affected responded to poliomyelitis vaccination with higher antibody titres, as if these children had already been exposed to an agent immunologically similar to poliomyelitis virus.<ref name=":02" /><ref>{{Cite journal|url=https://www.ncbi.nlm.nih.gov/pubmed/13515219|title=Response to poliomyelitis vaccination|last=Sigurdsson|first=B|author-link=Björn Sigurdsson|date=February 15, 1958|journal=The Lancet|volume=1|pages=370-1|via=}}</ref> During the 1949-1953 [[1949-53 Adelaide outbreak|outbreak in Adelaide]], cases of classic poliomyelitis dropped by 43%.<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2542300/ "Poliomyelitis in 1953"] ''Bulletin of the World Health Organization.'' 1955;12(4):595-649.</ref>   
There is indirect evidence of cross-immunity between [[poliovirus]] and the unidentified virus or viruses in epidemic myalgic encephalomyelitis outbreaks. After the 1948-1949 [[1948-49 Akureyri outbreak|Akureyri outbreak]] in Iceland, children in areas that had been affected responded to poliomyelitis vaccination with higher antibody titres, as if these children had already been exposed to an agent immunologically similar to poliomyelitis virus.<ref name=":02" /><ref>{{Cite journal|url=https://www.ncbi.nlm.nih.gov/pubmed/13515219| title = Response to poliomyelitis vaccination | last = Sigurdsson | first = B | author-link = Björn Sigurdsson | date = February 15, 1958|journal=The Lancet|volume=1|pages=370-1|via=}}</ref> During the 1949-1953 [[1949-53 Adelaide outbreak|outbreak in Adelaide]], cases of classic poliomyelitis dropped by 43%.<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2542300/ "Poliomyelitis in 1953"] ''Bulletin of the World Health Organization.'' 1955;12(4):595-649.</ref>   


== Post-polio syndrome ==
== Post-polio syndrome ==

Latest revision as of 16:26, April 3, 2023

Poliovirus is an enterovirus. It is the cause of the paralytic disease known as poliomyelitis."[1]

Poliovirus replication cycle
Source: Lévêque N, Semler BL (2015) A 21st Century Perspective of Poliovirus Replication. PLoS Pathog 11(6): e1004825. doi:10.1371/journal.ppat.1004825
© 2015 Lévêque, Semler CC-BY 4.0.

Metabolic effects[edit | edit source]

A study of poliovirus found that polio infection rapidly decreases (45% decrease) cellular oxygen consumption (and thus energy production through cellular respiration) by inhibiting succinate dehydrogenase (55% decrease in activity) and blocking mitochondrial electron transport at or between complexes I and III.[2]

Relationship to myalgic encephalomyelitis[edit | edit source]

Prior to the poliovirus vaccine, several outbreaks of what later came to be called myalgic encephalomyelitis coincided with confirmed outbreaks of poliomyelitis including the 1934 Los Angeles outbreak, the 1948 Akureyri, Iceland outbreak, and 1949 outbreak in Adelaide, Australia. Many outbreaks were initially misinterpreted as clusters of poliomyelitis or abortive poliomyelitis, hence one of ME's earliest names, atypical polio. It is not known whether there is a direct relationship between polio outbreaks and ME or if outbreaks of ME were more likely to be reported when public health authorities were already mobilized for an earlier crisis.

No serological evidence of polio was ever found in these outbreaks and the ultimate pattern of the outbreaks differed in significant ways, chief among them, the tendency to affect adults rather than children, and to result in higher morbidity than poliomyelitis but no mortality.[3] Findings in several outbreaks seemed to suggest that symptoms were caused by an enterovirus distinct from but related to polio including findings of mild, diffuse peripheral nervous system damage in monkeys infected with the virus; a stronger response to polio vaccination in children who had been in epidemic areas; and seasonal patterns of infection resembling polio.[3]

Cross-immunity[edit | edit source]

It is theorized that exposure to one enterovirus may confer partial immunity or improved immune response to another enteroviruses. One study compared schoolchildren in Estonia, who were inoculated with the Sabin, live attenuated virus polio vaccine, to Finnish schoolchildren, who were inoculated with the Salk, inactivated vaccine.[4] Estonian children had stronger T cell responses to coxsackievirus B4 and poliovirus type 1, and stronger expression of IFN-γ when exposed to poliovirus challenge as compared to Finnish children. Finnish children have weaker cellular immunity against enteroviruses at the age of 9 months compared with Estonian children at the same age. (Finland has a rate of type 1 diabetes three times the rate of Estonia. Coxsackie B4 has been associated with Type 1 diabetes.) An unintended consequence of widespread polio vaccination may have been impaired immunity to other enteroviruses, such as Coxsackie and echoviruses.

There is indirect evidence of cross-immunity between poliovirus and the unidentified virus or viruses in epidemic myalgic encephalomyelitis outbreaks. After the 1948-1949 Akureyri outbreak in Iceland, children in areas that had been affected responded to poliomyelitis vaccination with higher antibody titres, as if these children had already been exposed to an agent immunologically similar to poliomyelitis virus.[3][5] During the 1949-1953 outbreak in Adelaide, cases of classic poliomyelitis dropped by 43%.[6]

Post-polio syndrome[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. Poliovirus - Virology Blog
  2. Koundouris, A (May 2000). "Poliovirus Induces an Early Impairment of Mitochondrial Function by Inhibiting Succinate Dehydrogenase Activity". Biochemical and Biophysical Research Communications. 271: 610–4.
  3. 3.0 3.1 3.2 Parish, JG (1978). "Early outbreaks of 'epidemic neuromyasthenia'". Postgraduate Medical Journal. 54: 711–7.
  4. Juhela, S (July 1999). "Comparison of enterovirus-specific cellular immunity in two populations of young children vaccinated with inactivated or live poliovirus vaccines". Clinical & Experimental Immunology. 117: 100–105.
  5. Sigurdsson, B (February 15, 1958). "Response to poliomyelitis vaccination". The Lancet. 1: 370–1.
  6. "Poliomyelitis in 1953" Bulletin of the World Health Organization. 1955;12(4):595-649.