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This article is part of the Monkeypox outbreak task force, which is part of the WikiProject of Current events and this task force began in May 2022. Feel free to join and help! |
Hello to all who visit hereafter!
Thank you for reading, and please comment/criticize!-- FoodPuma ( talk) 19:49, 26 August 2008 (UTC)
Just wanted to suggest that the Monkeypox Disease be merged into the Monkeypox Virus page. Being that the Monkeypox Virus page in-and-of-itself is not justifiable as anymore than a stub, and that the Monkeypox Virus is the cause of the Disease, it makes sense to include the Disease under the main Monkeypox Virus page.
Please leave your thoughts and feelings on this as I feel merging the two topics into one would greatly improve their capability to assist Wikipedia users by condensing information into one place.-- FoodPuma ( talk) 21:37, 26 August 2008 (UTC)
Oppose merge: The virus & the disease are distinct entities. More & more is learned of each all the time. (I should know, I work in the field!) If merged, I think they would eventually need to be separated again. 140.139.35.250 ( talk) 21:26, 22 March 2009 (UTC)
Just wanted to call attention to a feature article from the WP on this subject that could serve other editors: here.
73.152.131.12 ( talk) 04:09, 5 November 2017 (UTC)
The following Wikimedia Commons file used on this page or its Wikidata item has been nominated for deletion:
Participate in the deletion discussion at the nomination page. — Community Tech bot ( talk) 17:36, 24 May 2022 (UTC)
The Monkeypox Virus and the Monkeypox pages should be merged in my opinion, much like the proposal a decade ago. While in some cases the division between disease and causative agent is useful (for instance Meningococcal being split from Meningitis, because other causative agents exist too), the only causative agent for Monkeypox is the Monkeypox Virus. Furthermore, with the natural zoonotic reservoir of the virus unidentified we are largely absent in discussion of the virus in other animals, the pages only really note that it's thought to have a zoonotic origin, and that it can be spread by a couple of other animals.
Additionally, the similarity of the page names is a source of confusion for non-experts, I do appreciate we have disambiguation pages but those are an imperfect solution, and we should bear in mind the possible confusion from highly similarly named pages.
I propose a merge of the pages, with a section dedicated to the nature of the virus outside of its infection itself.
If at some future point the pages need to be split off again due to some new development, so be it, but at present it this does not seem to be the case, and an argument about hypothetical future developments seems silly because Wikipedia doesn't work to a deadline.
The 2022 epidemic page should remain its own page however.
Please feel free to add your thoughts below. 5.151.23.56 ( talk) 09:18, 28 May 2022 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 18 August 2022 and 5 December 2022. Further details are available on the course page. Student editor(s): Solis.eve, ICapt.NemoI, Jap23630 ( article contribs). Peer reviewers: Meghanherlitzka, Acw66599, Microbio15, Walker16, Young416, Nathalieslebreton, Trinityt516, Egross123, Loganhardin, Dmancao7, Is73500, Ash0315, Jmoyang58, Zec57612.
— Assignment last updated by Jmoyang58 ( talk) 04:27, 21 October 2022 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 23 August 2022 and 15 December 2022. Further details are available on the course page. Student editor(s): FireWhirls, Celebrations18! ( article contribs). Peer reviewers: CraftWyvern, Error 4001.
— Assignment last updated by FloeEdge ( talk) 04:07, 20 October 2022 (UTC)
The sections "signs and symptoms", "prevention" and "treatment" are about the disease monkeypox rather than the virus (i.e. diseases have symptoms, prevention techniques, not viruses per se). It may be worth condensing these subsections into one single smaller section. For now I have put them all under one section "Monkeypox" and tagged with {{ Coatrack section}} so that it can be discussed here. Thanks. ArcMachaon ( talk) 19:48, 1 December 2022 (UTC)
User:Rreagan007, renaming the page was premature. The WHO do not name viruses or change their names. This is the responsibility of the International Committee on Taxonomy of Viruses who have not acted. See [1]. Graham Beards ( talk) 06:26, 31 January 2023 (UTC)
Moved. Treating this as a TR because consistency does not always override actual names found in reliable sources. If any editor thinks consistency is still more important, then they should consider a name change here to be controversial and open a fresh move request at any time. Thanks and kudos to the nom and other editors for your input; everyone stay healthy! P.I. Ellsworth , ed. put'r there 14:26, 31 January 2023 (UTC)
Mpox virus → Monkeypox virus – This page should be moved back to Monkeypox virus. Virus name changes are directed by the International Committee on Taxonomy of Viruses who have not changed the name of the genus. The move was not discussed and there is a re-direct. Graham Beards ( talk) 11:44, 31 January 2023 (UTC)
Have checked the most recent document from the International Committee on Taxonomy of Viruses dated 1 November 2022, and the species is still named "monkeypox virus". That is its official name and possibly still its common name. P.I. Ellsworth , ed. put'r there 16:39, 31 January 2023 (UTC)
I think this page needs thorough review and revision. Since the 2022 global outbreak, many reliable sources have been updated (e.g. WHO, CDC, Europa) and there has been new research and reviews which deserves to be included. Examples where the page is unsatisfactory:
There are other places where it's not good. Please can editors review recent reliable sources and update the page to match. Bob ( talk) 20:01, 2 June 2023 (UTC)
This
edit request has been answered. Set the |answered= or |ans= parameter to no to reactivate your request. |
Matusotruba ( talk) 11:07, 10 May 2024 (UTC)
Change heading "Immune system interaction" to "Immunological parameter of infection" then delete "Pox viruses have mechanisms to evade the hosts' innate and adaptive immune systems. Viral proteins, expressed by infected cells, employ multiple approaches to limit immune system activity; including binding to, and preventing activation of proteins within the host's immune system, and preventing infected cells from dying to enable them to continue replicating the monkey pox virus." and add From an immunological perspective, Monkeypox virus (MPXV) is an infection caused by a DNA virus belonging to the Orthopoxvirus family. Transmission occurs through direct contact with infected animals or humans, where the virus binds to cell surface saccharides (glycosaminoglycans) and enters cells via endocytosis. Despite its initial identification in Denmark in 1958, the immune response to this virus remains poorly characterized. Genomic analysis has shed light on the similarities between MPXV and Vaccinia virus, revealing a 92% nucleotide and 88% protein sequence similarity, particularly in immunologically significant proteins, thereby suggesting the presence of numerous shared immune epitopes [1]
The virus infiltrates epithelial cells, fibroblasts, and various immune cells including macrophages, monocytes, dendritic cells, and B or T-cells [2]. Innate immune cells serve as the primary responders to viral infections with macrophages and dendritic cells being particularly important, as they facilitate virus dissemination by migrating to lymph nodes, where the virus replicates [3]. This is followed by viral infection of human epidermal keratinocytes, as observed in vaccinia virus infections and induction of strong immunoregulatory cytokine production [4].
Natural killer cells, crucial components of innate immunity, undergo significant expansion during poxvirus infections, though their migratory and functional capacity can be impaired [5]. Furthermore, they play a protective role in controlling viral load, as demonstrated in mouse models with IL-15 treatment IL-15 increased the numbers of IFNγ-secreting natural killer cells and CD8+ T cells leading to the protective immunity in CAST/EiJ mice against lethal dose of MPXV infection [6]. Interestingly, natural killer cells are also involved in controlling other orthopoxvirus infections in mice, suggesting a conserved mechanism across species. Despite these insights, much remains unknown regarding the roles of various innate immune cells during human MPXV infection, highlighting the need for further research [7].
Endocytosed virus triggers innate immune responses via cytoplasmic DNA-sensing mechanisms including cGAS-STING pathway and Toll-like receptor (TLR) 9. Recognition of the virus in the cytoplasm leads to the activation Interferon regulatory factors (IRF) regulating transcription of interferons and nuclear factor kappa B (NF-κB) signaling pathways producing other inflammatory cytokines [8]. Production of dsRNA as the intermediates of viral replication activates protein kinase R (PKR) inhibiting protein translation of viral and cellular proteins via phosphorylation of eukaryotic initiation factor 2α (eIF2α) [9].
B cells and antibodies play a crucial role in combating poxviruses, with the type and magnitude of response influencing disease severity and vaccine effectiveness. Patients with moderate/severe disease often exhibit reduced anti-orthopoxvirus IgG responses, suggesting a correlation between antibody levels and disease severity [10]. An IgG-only response may indicate robust cross-protective memory B cells, while an IgM response could point out less effective primary immunity. Therefore, IgM responses might serve as a biomarker for disease severity, and identify vaccine candidates for protection.
T-cells play an importnant role in fighting poxvirus infections, especially CD4+ T cells, which help activate and differentiate memory B cells. Notably, vaccinia virus-specific CD4+ T cells have been shown to persist long-term and produce cytokines upon stimulation [11]. In contrast, CD4+ T cell deficiency can lead to severe MPXV infection, particularly in individuals with compromised immune systems [12]. CD8+ T cells, on the other hand, directly target infected cells, providing protection against viral spread and lethal infections. Despite the potential of T cell responses, smallpox vaccination may not confer robust immunity against MPXV, as evidenced by the absence of detectable T cell responses in some vaccinated individuals who were consequently infected with MPXV [13].
Since there is no treatment developed to treat MPXV disease and the mathematical model estimated a higher risk of contact spreading because of the limited herd immunity [14], pre-exposure profylaxis by a cross-protecting small-pox vaccine (currently available as a MPXV vaccine under the name IMVANEX) is highly recommended [15]. Its efficacy is likely attributed to the comparable humoral immune repsonses and recognizing different yet core set of poxvirus antigens mentioned earlier.
This suggestion can be further supported by the study published in 2023 quantifying neutralizing antibodies (NAbs) in sera from control, MPXV-infected, and modified vaccinia Ankara (MVA)-vaccinated individuals. 28-days after infection with MPXV, anti-MVA and -MPXV NAbs were observed in 94% and 82% of individuals, respectively Recipients recieving 2 doses of IMVANEX elicited anti-MVA and -MPXV NAbs in 92% and 56% of vaccinated individuals, respectively, and interestingly individuals born before 1980 vaccinated by a smallpox vaccine had increased levels of neutralizing antibodies against MPXV than younger individuals born after this year likely attributed to the prior smallpox vaccination recieved until 1980 and memory B-cell reactivation and antibody production [16]. — Preceding unsigned comment added by Matusotruba ( talk • contribs) 11:07, 10 May 2024 (UTC)
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This is the
talk page for discussing improvements to the
Monkeypox virus article. This is not a forum for general discussion of the article's subject. |
Article policies
|
Find medical sources: Source guidelines · PubMed · Cochrane · DOAJ · Gale · OpenMD · ScienceDirect · Springer · Trip · Wiley · TWL |
This article is rated C-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
This article is part of the Monkeypox outbreak task force, which is part of the WikiProject of Current events and this task force began in May 2022. Feel free to join and help! |
Hello to all who visit hereafter!
Thank you for reading, and please comment/criticize!-- FoodPuma ( talk) 19:49, 26 August 2008 (UTC)
Just wanted to suggest that the Monkeypox Disease be merged into the Monkeypox Virus page. Being that the Monkeypox Virus page in-and-of-itself is not justifiable as anymore than a stub, and that the Monkeypox Virus is the cause of the Disease, it makes sense to include the Disease under the main Monkeypox Virus page.
Please leave your thoughts and feelings on this as I feel merging the two topics into one would greatly improve their capability to assist Wikipedia users by condensing information into one place.-- FoodPuma ( talk) 21:37, 26 August 2008 (UTC)
Oppose merge: The virus & the disease are distinct entities. More & more is learned of each all the time. (I should know, I work in the field!) If merged, I think they would eventually need to be separated again. 140.139.35.250 ( talk) 21:26, 22 March 2009 (UTC)
Just wanted to call attention to a feature article from the WP on this subject that could serve other editors: here.
73.152.131.12 ( talk) 04:09, 5 November 2017 (UTC)
The following Wikimedia Commons file used on this page or its Wikidata item has been nominated for deletion:
Participate in the deletion discussion at the nomination page. — Community Tech bot ( talk) 17:36, 24 May 2022 (UTC)
The Monkeypox Virus and the Monkeypox pages should be merged in my opinion, much like the proposal a decade ago. While in some cases the division between disease and causative agent is useful (for instance Meningococcal being split from Meningitis, because other causative agents exist too), the only causative agent for Monkeypox is the Monkeypox Virus. Furthermore, with the natural zoonotic reservoir of the virus unidentified we are largely absent in discussion of the virus in other animals, the pages only really note that it's thought to have a zoonotic origin, and that it can be spread by a couple of other animals.
Additionally, the similarity of the page names is a source of confusion for non-experts, I do appreciate we have disambiguation pages but those are an imperfect solution, and we should bear in mind the possible confusion from highly similarly named pages.
I propose a merge of the pages, with a section dedicated to the nature of the virus outside of its infection itself.
If at some future point the pages need to be split off again due to some new development, so be it, but at present it this does not seem to be the case, and an argument about hypothetical future developments seems silly because Wikipedia doesn't work to a deadline.
The 2022 epidemic page should remain its own page however.
Please feel free to add your thoughts below. 5.151.23.56 ( talk) 09:18, 28 May 2022 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 18 August 2022 and 5 December 2022. Further details are available on the course page. Student editor(s): Solis.eve, ICapt.NemoI, Jap23630 ( article contribs). Peer reviewers: Meghanherlitzka, Acw66599, Microbio15, Walker16, Young416, Nathalieslebreton, Trinityt516, Egross123, Loganhardin, Dmancao7, Is73500, Ash0315, Jmoyang58, Zec57612.
— Assignment last updated by Jmoyang58 ( talk) 04:27, 21 October 2022 (UTC)
This article was the subject of a Wiki Education Foundation-supported course assignment, between 23 August 2022 and 15 December 2022. Further details are available on the course page. Student editor(s): FireWhirls, Celebrations18! ( article contribs). Peer reviewers: CraftWyvern, Error 4001.
— Assignment last updated by FloeEdge ( talk) 04:07, 20 October 2022 (UTC)
The sections "signs and symptoms", "prevention" and "treatment" are about the disease monkeypox rather than the virus (i.e. diseases have symptoms, prevention techniques, not viruses per se). It may be worth condensing these subsections into one single smaller section. For now I have put them all under one section "Monkeypox" and tagged with {{ Coatrack section}} so that it can be discussed here. Thanks. ArcMachaon ( talk) 19:48, 1 December 2022 (UTC)
User:Rreagan007, renaming the page was premature. The WHO do not name viruses or change their names. This is the responsibility of the International Committee on Taxonomy of Viruses who have not acted. See [1]. Graham Beards ( talk) 06:26, 31 January 2023 (UTC)
Moved. Treating this as a TR because consistency does not always override actual names found in reliable sources. If any editor thinks consistency is still more important, then they should consider a name change here to be controversial and open a fresh move request at any time. Thanks and kudos to the nom and other editors for your input; everyone stay healthy! P.I. Ellsworth , ed. put'r there 14:26, 31 January 2023 (UTC)
Mpox virus → Monkeypox virus – This page should be moved back to Monkeypox virus. Virus name changes are directed by the International Committee on Taxonomy of Viruses who have not changed the name of the genus. The move was not discussed and there is a re-direct. Graham Beards ( talk) 11:44, 31 January 2023 (UTC)
Have checked the most recent document from the International Committee on Taxonomy of Viruses dated 1 November 2022, and the species is still named "monkeypox virus". That is its official name and possibly still its common name. P.I. Ellsworth , ed. put'r there 16:39, 31 January 2023 (UTC)
I think this page needs thorough review and revision. Since the 2022 global outbreak, many reliable sources have been updated (e.g. WHO, CDC, Europa) and there has been new research and reviews which deserves to be included. Examples where the page is unsatisfactory:
There are other places where it's not good. Please can editors review recent reliable sources and update the page to match. Bob ( talk) 20:01, 2 June 2023 (UTC)
This
edit request has been answered. Set the |answered= or |ans= parameter to no to reactivate your request. |
Matusotruba ( talk) 11:07, 10 May 2024 (UTC)
Change heading "Immune system interaction" to "Immunological parameter of infection" then delete "Pox viruses have mechanisms to evade the hosts' innate and adaptive immune systems. Viral proteins, expressed by infected cells, employ multiple approaches to limit immune system activity; including binding to, and preventing activation of proteins within the host's immune system, and preventing infected cells from dying to enable them to continue replicating the monkey pox virus." and add From an immunological perspective, Monkeypox virus (MPXV) is an infection caused by a DNA virus belonging to the Orthopoxvirus family. Transmission occurs through direct contact with infected animals or humans, where the virus binds to cell surface saccharides (glycosaminoglycans) and enters cells via endocytosis. Despite its initial identification in Denmark in 1958, the immune response to this virus remains poorly characterized. Genomic analysis has shed light on the similarities between MPXV and Vaccinia virus, revealing a 92% nucleotide and 88% protein sequence similarity, particularly in immunologically significant proteins, thereby suggesting the presence of numerous shared immune epitopes [1]
The virus infiltrates epithelial cells, fibroblasts, and various immune cells including macrophages, monocytes, dendritic cells, and B or T-cells [2]. Innate immune cells serve as the primary responders to viral infections with macrophages and dendritic cells being particularly important, as they facilitate virus dissemination by migrating to lymph nodes, where the virus replicates [3]. This is followed by viral infection of human epidermal keratinocytes, as observed in vaccinia virus infections and induction of strong immunoregulatory cytokine production [4].
Natural killer cells, crucial components of innate immunity, undergo significant expansion during poxvirus infections, though their migratory and functional capacity can be impaired [5]. Furthermore, they play a protective role in controlling viral load, as demonstrated in mouse models with IL-15 treatment IL-15 increased the numbers of IFNγ-secreting natural killer cells and CD8+ T cells leading to the protective immunity in CAST/EiJ mice against lethal dose of MPXV infection [6]. Interestingly, natural killer cells are also involved in controlling other orthopoxvirus infections in mice, suggesting a conserved mechanism across species. Despite these insights, much remains unknown regarding the roles of various innate immune cells during human MPXV infection, highlighting the need for further research [7].
Endocytosed virus triggers innate immune responses via cytoplasmic DNA-sensing mechanisms including cGAS-STING pathway and Toll-like receptor (TLR) 9. Recognition of the virus in the cytoplasm leads to the activation Interferon regulatory factors (IRF) regulating transcription of interferons and nuclear factor kappa B (NF-κB) signaling pathways producing other inflammatory cytokines [8]. Production of dsRNA as the intermediates of viral replication activates protein kinase R (PKR) inhibiting protein translation of viral and cellular proteins via phosphorylation of eukaryotic initiation factor 2α (eIF2α) [9].
B cells and antibodies play a crucial role in combating poxviruses, with the type and magnitude of response influencing disease severity and vaccine effectiveness. Patients with moderate/severe disease often exhibit reduced anti-orthopoxvirus IgG responses, suggesting a correlation between antibody levels and disease severity [10]. An IgG-only response may indicate robust cross-protective memory B cells, while an IgM response could point out less effective primary immunity. Therefore, IgM responses might serve as a biomarker for disease severity, and identify vaccine candidates for protection.
T-cells play an importnant role in fighting poxvirus infections, especially CD4+ T cells, which help activate and differentiate memory B cells. Notably, vaccinia virus-specific CD4+ T cells have been shown to persist long-term and produce cytokines upon stimulation [11]. In contrast, CD4+ T cell deficiency can lead to severe MPXV infection, particularly in individuals with compromised immune systems [12]. CD8+ T cells, on the other hand, directly target infected cells, providing protection against viral spread and lethal infections. Despite the potential of T cell responses, smallpox vaccination may not confer robust immunity against MPXV, as evidenced by the absence of detectable T cell responses in some vaccinated individuals who were consequently infected with MPXV [13].
Since there is no treatment developed to treat MPXV disease and the mathematical model estimated a higher risk of contact spreading because of the limited herd immunity [14], pre-exposure profylaxis by a cross-protecting small-pox vaccine (currently available as a MPXV vaccine under the name IMVANEX) is highly recommended [15]. Its efficacy is likely attributed to the comparable humoral immune repsonses and recognizing different yet core set of poxvirus antigens mentioned earlier.
This suggestion can be further supported by the study published in 2023 quantifying neutralizing antibodies (NAbs) in sera from control, MPXV-infected, and modified vaccinia Ankara (MVA)-vaccinated individuals. 28-days after infection with MPXV, anti-MVA and -MPXV NAbs were observed in 94% and 82% of individuals, respectively Recipients recieving 2 doses of IMVANEX elicited anti-MVA and -MPXV NAbs in 92% and 56% of vaccinated individuals, respectively, and interestingly individuals born before 1980 vaccinated by a smallpox vaccine had increased levels of neutralizing antibodies against MPXV than younger individuals born after this year likely attributed to the prior smallpox vaccination recieved until 1980 and memory B-cell reactivation and antibody production [16]. — Preceding unsigned comment added by Matusotruba ( talk • contribs) 11:07, 10 May 2024 (UTC)
References
{{
cite journal}}
: Check |doi=
value (
help); External link in |doi=
(
help)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: CS1 maint: unflagged free DOI (
link)
{{
cite journal}}
: Check |doi=
value (
help); External link in |doi=
(
help)
{{
cite web}}
: Missing or empty |title=
(
help)
{{
cite journal}}
: Check |doi=
value (
help); External link in |doi=
(
help)
{{
cite journal}}
: Check |doi=
value (
help); External link in |doi=
(
help)