The virus was identified in 1958 in experimental monkeys in Denmark, and the first human Monkeypox instance was documented in 1970 in the Republic of the Congo (DRC). The virus is generally zoonotic, implying it primarily infects animals but can also affect people. The virus is mainly found in Central and West African tropical forests.
Rodents, notably squirrels and monkeys, are thought to be the actual reservoirs and hosts of the Monkeypox virus. Human infections arise due to close contacts with sick animals, like handling bodily fluids or meat, or because of bites or scratches. Furthermore, transmission from person to person can occur via direct contact with respiratory aerosols or fluid from infected persons’ skin sores.
Monkeypox appeared irregularly in Central & Eastern Africa (clade I) and the West African region (clade II) around 1970. An epidemic in the USA in 2003 was traced back to smuggled wild animals (clade II). Between October and December of 2005, ten proven and nine potential cases of Monkeypox were reported in five villages in Unity State, Sudan: three in Modin, two in Bentiu, five in Rubkona, five in Nuria, and four in Wang Kay. In 2017, mpox resurfaced in Nigeria and has since spread throughout and among visitors to other countries.
In May 2022, a Monkeypox outbreak erupted and quickly expanded over Europe, North America, and all six WHO territories, with 110 countries confirming approximately 87000 cases and 112 casualties. The global outbreak mainly had (but not exclusively) afflicted bisexual, gay, and similar males who engage in sex with men & has spread between individuals via sexual contact. On 23 July 2022, the global Monkeypox outbreak was declared a health emergency with global significance.
  Kingdom: Virus
  Phylum: Nucleocytoviricota
  Class: Pokkesviricetes
  Order: Chitovirales
  Family: Poxviridae
  Genus: Orthopoxvirus
  Species: Monkeypox virus
Monkeypox virus has a complicated structure comprised of a brick-shaped envelope that encapsulates a massive, double-stranded DNA genome that measures 200 to 250 nm in diameter.
The virus is covered by an outer lipid envelope derived from the host cell membrane. This envelope is studded with viral glycoproteins. Inside the envelope are a proteinaceous core containing the viral genome and various viral enzymes required for replication and transcription. The core is surrounded by a protein layer called the tegument.
The Monkeypox viral genome is roughly 200kb long and codes about 200 proteins. It is around 197 kb and contains 190 different Open Read frames.
There are two antigenic kinds of Monkeypox virus: the West African clade & the Congo Basin clade. The West African lineage has a milder clinical appearance with fatality rates of 3.6% (94% CI 1.5-6.9%), whereas the Congo Basin clade tends to be more pathogenic with a fatality proportion of 10.7% (94% CI 8.6-13.4%) and increased human-to-human transmission.
Vaccines produced against the West African lineage of Monkeypox virus are not equally effective against the Congo Basin lineage.
When compared to other viruses, the Monkeypox virus appears quite big. It makes it more difficult for the pathogen to penetrate host defenses, such as bridging gap junctions. Furthermore, the virus’s colossal size makes it more challenging to multiply quickly and elude immune reaction.
Monkeypox viruses have adapted to avoid host defense systems by coding for both internal and exogenous modulatory proteins. The Monkeypox virus replicates rapidly in lymphoid organs. Clinical investigations of human Monkeypox indicate that lymphoid cells in the neck & throat are the main sites of MPXV replication.
The Monkeypox virus has numerous surface proteins that aid in its passage into host tissues; the virus can merge with host cells through 10-12 transmembrane proteins. On the cell surface, it most likely attaches to laminin or glycosaminoglycans.
Monkeypox virus can spread to other organs through the lymphohaematogenous pathway after developing low-grade primary viremia because of infection of lymphoid tissues. Virus infection in these tissues causes a second large viremia wave, which spreads the virus across the kidneys, lungs, intestinal tract, skin, & other systems. The Monkeypox virus within the small dermal veins signals the initial stage of skin infections and the formation of skin lesions.
Viral shedding has also been observed in feces, suggesting that interaction with the mucosa of the rectal may increase the risk of MPXV transmission. It was previously discovered in patients with the type 1 human immunodeficiency virus, suggesting such tissue could serve as a virus reservoir. A recent study discovered that the immunological milieu of the rectal mucosa in MSM differed significantly from that of heterosexual persons, with a greater incidence of immune responses indicative of mucosal damage.
IgM antibodies primarily drive the primary immune response. The IgM-dominated primary response is slower and less efficient in controlling the infection than the secondary IgG response. A robust IgG+ memory B cell population ensures a rapid and effective immune response upon re-exposure to the virus, producing specific IgG antibodies that confer protection against Monkeypox virus infection.
Susceptible monocytes, specifically CD14+ monocytes, are actively recruited to the sites of infection CD14+ monocytes are a subset of monocytes that express the CD14 cell surface marker; the expansion of CD14+ monocytes in the lungs indicates their active involvement in the immune response against Monkeypox virus.
Ly6G+ monocytes, a subset of monocytes expressing the Ly6G cell surface marker, also play a role in the immune response against the Monkeypox virus. By infiltrating the infected tissues, Ly6G+ monocytes contribute to the clearance of the Monkeypox virus and the resolution of infection.
A downregulation of chemokine receptors such as CXCR3, CCR5, CCR6, and CCR7 on immune cells has been observed in host defense against the Monkeypox virus. They enable immune cells to respond to specific chemokines produced at the site of infection and facilitate their recruitment to the affected tissues. By downregulating these chemokine receptors, the Monkeypox virus can hinder the recruitment of immune cells that are critical for the control and clearance of the infection.
During Monkeypox virus infection, infected cells present viral antigens on their MHC class I molecules, including the Qa-1b peptide complex. NK cells expressing NKG2E and CD94 receptors can recognize and bind to these complexes, triggering an immune response. The NKG2E and CD94 receptors binding to the Qa-1b peptide complex on infected cells leads to NK cell activation and subsequent release of cytotoxic molecules, such as perforin and granzymes. These cytotoxic molecules can induce cell death in the infected cells, limiting viral replication and spread. By engaging NKG2E and CD94 receptors, NK cells can directly target and eliminate Monkeypox virus-infected cells, contributing to the host defense against the virus.
Monkeypox is the primary disease caused by Monkeypox virus in humans. It typically manifests as a febrile illness with a rash. The clinical course of Monkeypox can vary from mild to severe. The typical clinical manifestations of Monkeypox virus infection include:
Skin Lesions: The most characteristic feature of Monkeypox infection is the development of skin lesions. These lesions progress through different stages, starting as a rash of papules (small, raised bumps) that later develop into vesicles (fluid-filled blisters) and eventually form pustules (pus-filled blisters). These lesions can be widespread across the body and often involve the face, palms of the hands, and soles of the feet.
Fever: Monkeypox infection is usually accompanied by fever, often high-grade and persistent. The fever may precede the appearance of skin lesions.
Lymphadenopathy: Swelling of the lymph nodes, referred to as lymphadenopathy, is commonly observed in Monkeypox infection. The affected lymph nodes may become enlarged, tender, and palpable.
Polymerase chain reaction method: The process begins by extracting the viral genetic material from clinical samples, such as skin lesions or respiratory secretions, and then subjecting it to PCR amplification using specific primers that target regions of the Monkeypox virus genome, the genes commonly targeted for conventional PCR testing of Monkeypox virus include hemagglutinin, the acidophilic-type inclusion body gene, and the crmB gene. These genes are specific to the Monkeypox virus and can serve as reliable markers for its detection. PCR primers designed to amplify regions within these genes can amplify and detect Monkeypox virus DNA in clinical samples. By targeting multiple genes, PCR testing enhances the sensitivity and specificity of the diagnostic assay, allowing for accurate identification of Monkeypox virus infection.
Western blot technique: The viral proteins present in the sample are separated based on their molecular weight using gel electrophoresis. The proteins are loaded onto a polyacrylamide gel and subjected to an electric field, causing them to migrate through the gel matrix. The separated proteins are transferred onto a solid membrane, typically made of nitrocellulose or polyvinylidene fluoride. After transfer, the membrane is blocked with a protein-blocking agent to prevent non-specific binding. Specific antibodies that recognize the target viral proteins are added to the membrane. If present in the sample, these primary antibodies will bind to the corresponding viral proteins. To visualize the bound antibodies, a secondary antibody is added. This secondary antibody is linked with a fluorescent dye or an enzyme. When exposed to a specific substrate, the enzyme generates a detectable signal, while the fluorescent dye emits light of a specific wavelength when excited by appropriate light. The presence of the viral proteins is indicated by bands on the membrane, which correspond to the specific target proteins. The intensity of the bands can be correlated with the amount of viral protein present in the sample.
Enzyme-linked immunosorbent assay: It is the most widely used diagnostic technique for detecting Monkeypox virus-specific antibodies in patient serum. In ELISA, the virus-specific antigens are immobilized onto a solid surface, such as a microplate, and then the patient’s serum is added. If antibodies against the Monkeypox virus are present in the serum, they react to the immobilized antigens. This binding is detected using an enzyme-linked secondary antibody that produces a colorimetric signal, indicating the presence of Monkeypox virus-specific antibodies.
Keep skin dry and uncovered (unless in a room with someone else): This practice can help reduce moisture and promote the healing of skin lesions. It may also restrict the spread of infection to others, as direct skin-to-skin contact can facilitate transmission.
Avoid touching items in shared spaces and disinfect shared spaces frequently: Monkeypox virus can survive on surfaces for a certain period. You can minimize the risk of indirect transmission by avoiding unnecessary contact with shared items and frequently disinfecting commonly touched surfaces.
Use saltwater rinses for sores in the mouth: Saltwater rinses can temporarily relieve mouth sores associated with Monkeypox virus infection. They can help cleanse the mouth, reduce inflammation, and promote healing. However, seeking medical advice to manage oral symptoms appropriately is essential.
Take sitz baths or warm baths with baking soda or Epsom salts for body sores: Soaking in sitz baths or warm baths with Epsom salts or baking soda can soothe discomfort associated with body sores. It can provide relief from itching, reduce inflammation, and promote healing.
Mpox (Monkeypox) (who.int)
Monkeypox: epidemiology, pathogenesis, treatment and prevention | Signal Transduction and Targeted Therapy (nature.com)
The virus was identified in 1958 in experimental monkeys in Denmark, and the first human Monkeypox instance was documented in 1970 in the Republic of the Congo (DRC). The virus is generally zoonotic, implying it primarily infects animals but can also affect people. The virus is mainly found in Central and West African tropical forests.
Rodents, notably squirrels and monkeys, are thought to be the actual reservoirs and hosts of the Monkeypox virus. Human infections arise due to close contacts with sick animals, like handling bodily fluids or meat, or because of bites or scratches. Furthermore, transmission from person to person can occur via direct contact with respiratory aerosols or fluid from infected persons’ skin sores.
Monkeypox appeared irregularly in Central & Eastern Africa (clade I) and the West African region (clade II) around 1970. An epidemic in the USA in 2003 was traced back to smuggled wild animals (clade II). Between October and December of 2005, ten proven and nine potential cases of Monkeypox were reported in five villages in Unity State, Sudan: three in Modin, two in Bentiu, five in Rubkona, five in Nuria, and four in Wang Kay. In 2017, mpox resurfaced in Nigeria and has since spread throughout and among visitors to other countries.
In May 2022, a Monkeypox outbreak erupted and quickly expanded over Europe, North America, and all six WHO territories, with 110 countries confirming approximately 87000 cases and 112 casualties. The global outbreak mainly had (but not exclusively) afflicted bisexual, gay, and similar males who engage in sex with men & has spread between individuals via sexual contact. On 23 July 2022, the global Monkeypox outbreak was declared a health emergency with global significance.
  Kingdom: Virus
  Phylum: Nucleocytoviricota
  Class: Pokkesviricetes
  Order: Chitovirales
  Family: Poxviridae
  Genus: Orthopoxvirus
  Species: Monkeypox virus
Monkeypox virus has a complicated structure comprised of a brick-shaped envelope that encapsulates a massive, double-stranded DNA genome that measures 200 to 250 nm in diameter.
The virus is covered by an outer lipid envelope derived from the host cell membrane. This envelope is studded with viral glycoproteins. Inside the envelope are a proteinaceous core containing the viral genome and various viral enzymes required for replication and transcription. The core is surrounded by a protein layer called the tegument.
The Monkeypox viral genome is roughly 200kb long and codes about 200 proteins. It is around 197 kb and contains 190 different Open Read frames.
There are two antigenic kinds of Monkeypox virus: the West African clade & the Congo Basin clade. The West African lineage has a milder clinical appearance with fatality rates of 3.6% (94% CI 1.5-6.9%), whereas the Congo Basin clade tends to be more pathogenic with a fatality proportion of 10.7% (94% CI 8.6-13.4%) and increased human-to-human transmission.
Vaccines produced against the West African lineage of Monkeypox virus are not equally effective against the Congo Basin lineage.
When compared to other viruses, the Monkeypox virus appears quite big. It makes it more difficult for the pathogen to penetrate host defenses, such as bridging gap junctions. Furthermore, the virus’s colossal size makes it more challenging to multiply quickly and elude immune reaction.
Monkeypox viruses have adapted to avoid host defense systems by coding for both internal and exogenous modulatory proteins. The Monkeypox virus replicates rapidly in lymphoid organs. Clinical investigations of human Monkeypox indicate that lymphoid cells in the neck & throat are the main sites of MPXV replication.
The Monkeypox virus has numerous surface proteins that aid in its passage into host tissues; the virus can merge with host cells through 10-12 transmembrane proteins. On the cell surface, it most likely attaches to laminin or glycosaminoglycans.
Monkeypox virus can spread to other organs through the lymphohaematogenous pathway after developing low-grade primary viremia because of infection of lymphoid tissues. Virus infection in these tissues causes a second large viremia wave, which spreads the virus across the kidneys, lungs, intestinal tract, skin, & other systems. The Monkeypox virus within the small dermal veins signals the initial stage of skin infections and the formation of skin lesions.
Viral shedding has also been observed in feces, suggesting that interaction with the mucosa of the rectal may increase the risk of MPXV transmission. It was previously discovered in patients with the type 1 human immunodeficiency virus, suggesting such tissue could serve as a virus reservoir. A recent study discovered that the immunological milieu of the rectal mucosa in MSM differed significantly from that of heterosexual persons, with a greater incidence of immune responses indicative of mucosal damage.
IgM antibodies primarily drive the primary immune response. The IgM-dominated primary response is slower and less efficient in controlling the infection than the secondary IgG response. A robust IgG+ memory B cell population ensures a rapid and effective immune response upon re-exposure to the virus, producing specific IgG antibodies that confer protection against Monkeypox virus infection.
Susceptible monocytes, specifically CD14+ monocytes, are actively recruited to the sites of infection CD14+ monocytes are a subset of monocytes that express the CD14 cell surface marker; the expansion of CD14+ monocytes in the lungs indicates their active involvement in the immune response against Monkeypox virus.
Ly6G+ monocytes, a subset of monocytes expressing the Ly6G cell surface marker, also play a role in the immune response against the Monkeypox virus. By infiltrating the infected tissues, Ly6G+ monocytes contribute to the clearance of the Monkeypox virus and the resolution of infection.
A downregulation of chemokine receptors such as CXCR3, CCR5, CCR6, and CCR7 on immune cells has been observed in host defense against the Monkeypox virus. They enable immune cells to respond to specific chemokines produced at the site of infection and facilitate their recruitment to the affected tissues. By downregulating these chemokine receptors, the Monkeypox virus can hinder the recruitment of immune cells that are critical for the control and clearance of the infection.
During Monkeypox virus infection, infected cells present viral antigens on their MHC class I molecules, including the Qa-1b peptide complex. NK cells expressing NKG2E and CD94 receptors can recognize and bind to these complexes, triggering an immune response. The NKG2E and CD94 receptors binding to the Qa-1b peptide complex on infected cells leads to NK cell activation and subsequent release of cytotoxic molecules, such as perforin and granzymes. These cytotoxic molecules can induce cell death in the infected cells, limiting viral replication and spread. By engaging NKG2E and CD94 receptors, NK cells can directly target and eliminate Monkeypox virus-infected cells, contributing to the host defense against the virus.
Monkeypox is the primary disease caused by Monkeypox virus in humans. It typically manifests as a febrile illness with a rash. The clinical course of Monkeypox can vary from mild to severe. The typical clinical manifestations of Monkeypox virus infection include:
Skin Lesions: The most characteristic feature of Monkeypox infection is the development of skin lesions. These lesions progress through different stages, starting as a rash of papules (small, raised bumps) that later develop into vesicles (fluid-filled blisters) and eventually form pustules (pus-filled blisters). These lesions can be widespread across the body and often involve the face, palms of the hands, and soles of the feet.
Fever: Monkeypox infection is usually accompanied by fever, often high-grade and persistent. The fever may precede the appearance of skin lesions.
Lymphadenopathy: Swelling of the lymph nodes, referred to as lymphadenopathy, is commonly observed in Monkeypox infection. The affected lymph nodes may become enlarged, tender, and palpable.
Polymerase chain reaction method: The process begins by extracting the viral genetic material from clinical samples, such as skin lesions or respiratory secretions, and then subjecting it to PCR amplification using specific primers that target regions of the Monkeypox virus genome, the genes commonly targeted for conventional PCR testing of Monkeypox virus include hemagglutinin, the acidophilic-type inclusion body gene, and the crmB gene. These genes are specific to the Monkeypox virus and can serve as reliable markers for its detection. PCR primers designed to amplify regions within these genes can amplify and detect Monkeypox virus DNA in clinical samples. By targeting multiple genes, PCR testing enhances the sensitivity and specificity of the diagnostic assay, allowing for accurate identification of Monkeypox virus infection.
Western blot technique: The viral proteins present in the sample are separated based on their molecular weight using gel electrophoresis. The proteins are loaded onto a polyacrylamide gel and subjected to an electric field, causing them to migrate through the gel matrix. The separated proteins are transferred onto a solid membrane, typically made of nitrocellulose or polyvinylidene fluoride. After transfer, the membrane is blocked with a protein-blocking agent to prevent non-specific binding. Specific antibodies that recognize the target viral proteins are added to the membrane. If present in the sample, these primary antibodies will bind to the corresponding viral proteins. To visualize the bound antibodies, a secondary antibody is added. This secondary antibody is linked with a fluorescent dye or an enzyme. When exposed to a specific substrate, the enzyme generates a detectable signal, while the fluorescent dye emits light of a specific wavelength when excited by appropriate light. The presence of the viral proteins is indicated by bands on the membrane, which correspond to the specific target proteins. The intensity of the bands can be correlated with the amount of viral protein present in the sample.
Enzyme-linked immunosorbent assay: It is the most widely used diagnostic technique for detecting Monkeypox virus-specific antibodies in patient serum. In ELISA, the virus-specific antigens are immobilized onto a solid surface, such as a microplate, and then the patient’s serum is added. If antibodies against the Monkeypox virus are present in the serum, they react to the immobilized antigens. This binding is detected using an enzyme-linked secondary antibody that produces a colorimetric signal, indicating the presence of Monkeypox virus-specific antibodies.
Keep skin dry and uncovered (unless in a room with someone else): This practice can help reduce moisture and promote the healing of skin lesions. It may also restrict the spread of infection to others, as direct skin-to-skin contact can facilitate transmission.
Avoid touching items in shared spaces and disinfect shared spaces frequently: Monkeypox virus can survive on surfaces for a certain period. You can minimize the risk of indirect transmission by avoiding unnecessary contact with shared items and frequently disinfecting commonly touched surfaces.
Use saltwater rinses for sores in the mouth: Saltwater rinses can temporarily relieve mouth sores associated with Monkeypox virus infection. They can help cleanse the mouth, reduce inflammation, and promote healing. However, seeking medical advice to manage oral symptoms appropriately is essential.
Take sitz baths or warm baths with baking soda or Epsom salts for body sores: Soaking in sitz baths or warm baths with Epsom salts or baking soda can soothe discomfort associated with body sores. It can provide relief from itching, reduce inflammation, and promote healing.
Mpox (Monkeypox) (who.int)
Monkeypox: epidemiology, pathogenesis, treatment and prevention | Signal Transduction and Targeted Therapy (nature.com)
The virus was identified in 1958 in experimental monkeys in Denmark, and the first human Monkeypox instance was documented in 1970 in the Republic of the Congo (DRC). The virus is generally zoonotic, implying it primarily infects animals but can also affect people. The virus is mainly found in Central and West African tropical forests.
Rodents, notably squirrels and monkeys, are thought to be the actual reservoirs and hosts of the Monkeypox virus. Human infections arise due to close contacts with sick animals, like handling bodily fluids or meat, or because of bites or scratches. Furthermore, transmission from person to person can occur via direct contact with respiratory aerosols or fluid from infected persons’ skin sores.
Monkeypox appeared irregularly in Central & Eastern Africa (clade I) and the West African region (clade II) around 1970. An epidemic in the USA in 2003 was traced back to smuggled wild animals (clade II). Between October and December of 2005, ten proven and nine potential cases of Monkeypox were reported in five villages in Unity State, Sudan: three in Modin, two in Bentiu, five in Rubkona, five in Nuria, and four in Wang Kay. In 2017, mpox resurfaced in Nigeria and has since spread throughout and among visitors to other countries.
In May 2022, a Monkeypox outbreak erupted and quickly expanded over Europe, North America, and all six WHO territories, with 110 countries confirming approximately 87000 cases and 112 casualties. The global outbreak mainly had (but not exclusively) afflicted bisexual, gay, and similar males who engage in sex with men & has spread between individuals via sexual contact. On 23 July 2022, the global Monkeypox outbreak was declared a health emergency with global significance.
  Kingdom: Virus
  Phylum: Nucleocytoviricota
  Class: Pokkesviricetes
  Order: Chitovirales
  Family: Poxviridae
  Genus: Orthopoxvirus
  Species: Monkeypox virus
Monkeypox virus has a complicated structure comprised of a brick-shaped envelope that encapsulates a massive, double-stranded DNA genome that measures 200 to 250 nm in diameter.
The virus is covered by an outer lipid envelope derived from the host cell membrane. This envelope is studded with viral glycoproteins. Inside the envelope are a proteinaceous core containing the viral genome and various viral enzymes required for replication and transcription. The core is surrounded by a protein layer called the tegument.
The Monkeypox viral genome is roughly 200kb long and codes about 200 proteins. It is around 197 kb and contains 190 different Open Read frames.
There are two antigenic kinds of Monkeypox virus: the West African clade & the Congo Basin clade. The West African lineage has a milder clinical appearance with fatality rates of 3.6% (94% CI 1.5-6.9%), whereas the Congo Basin clade tends to be more pathogenic with a fatality proportion of 10.7% (94% CI 8.6-13.4%) and increased human-to-human transmission.
Vaccines produced against the West African lineage of Monkeypox virus are not equally effective against the Congo Basin lineage.
When compared to other viruses, the Monkeypox virus appears quite big. It makes it more difficult for the pathogen to penetrate host defenses, such as bridging gap junctions. Furthermore, the virus’s colossal size makes it more challenging to multiply quickly and elude immune reaction.
Monkeypox viruses have adapted to avoid host defense systems by coding for both internal and exogenous modulatory proteins. The Monkeypox virus replicates rapidly in lymphoid organs. Clinical investigations of human Monkeypox indicate that lymphoid cells in the neck & throat are the main sites of MPXV replication.
The Monkeypox virus has numerous surface proteins that aid in its passage into host tissues; the virus can merge with host cells through 10-12 transmembrane proteins. On the cell surface, it most likely attaches to laminin or glycosaminoglycans.
Monkeypox virus can spread to other organs through the lymphohaematogenous pathway after developing low-grade primary viremia because of infection of lymphoid tissues. Virus infection in these tissues causes a second large viremia wave, which spreads the virus across the kidneys, lungs, intestinal tract, skin, & other systems. The Monkeypox virus within the small dermal veins signals the initial stage of skin infections and the formation of skin lesions.
Viral shedding has also been observed in feces, suggesting that interaction with the mucosa of the rectal may increase the risk of MPXV transmission. It was previously discovered in patients with the type 1 human immunodeficiency virus, suggesting such tissue could serve as a virus reservoir. A recent study discovered that the immunological milieu of the rectal mucosa in MSM differed significantly from that of heterosexual persons, with a greater incidence of immune responses indicative of mucosal damage.
IgM antibodies primarily drive the primary immune response. The IgM-dominated primary response is slower and less efficient in controlling the infection than the secondary IgG response. A robust IgG+ memory B cell population ensures a rapid and effective immune response upon re-exposure to the virus, producing specific IgG antibodies that confer protection against Monkeypox virus infection.
Susceptible monocytes, specifically CD14+ monocytes, are actively recruited to the sites of infection CD14+ monocytes are a subset of monocytes that express the CD14 cell surface marker; the expansion of CD14+ monocytes in the lungs indicates their active involvement in the immune response against Monkeypox virus.
Ly6G+ monocytes, a subset of monocytes expressing the Ly6G cell surface marker, also play a role in the immune response against the Monkeypox virus. By infiltrating the infected tissues, Ly6G+ monocytes contribute to the clearance of the Monkeypox virus and the resolution of infection.
A downregulation of chemokine receptors such as CXCR3, CCR5, CCR6, and CCR7 on immune cells has been observed in host defense against the Monkeypox virus. They enable immune cells to respond to specific chemokines produced at the site of infection and facilitate their recruitment to the affected tissues. By downregulating these chemokine receptors, the Monkeypox virus can hinder the recruitment of immune cells that are critical for the control and clearance of the infection.
During Monkeypox virus infection, infected cells present viral antigens on their MHC class I molecules, including the Qa-1b peptide complex. NK cells expressing NKG2E and CD94 receptors can recognize and bind to these complexes, triggering an immune response. The NKG2E and CD94 receptors binding to the Qa-1b peptide complex on infected cells leads to NK cell activation and subsequent release of cytotoxic molecules, such as perforin and granzymes. These cytotoxic molecules can induce cell death in the infected cells, limiting viral replication and spread. By engaging NKG2E and CD94 receptors, NK cells can directly target and eliminate Monkeypox virus-infected cells, contributing to the host defense against the virus.
Monkeypox is the primary disease caused by Monkeypox virus in humans. It typically manifests as a febrile illness with a rash. The clinical course of Monkeypox can vary from mild to severe. The typical clinical manifestations of Monkeypox virus infection include:
Skin Lesions: The most characteristic feature of Monkeypox infection is the development of skin lesions. These lesions progress through different stages, starting as a rash of papules (small, raised bumps) that later develop into vesicles (fluid-filled blisters) and eventually form pustules (pus-filled blisters). These lesions can be widespread across the body and often involve the face, palms of the hands, and soles of the feet.
Fever: Monkeypox infection is usually accompanied by fever, often high-grade and persistent. The fever may precede the appearance of skin lesions.
Lymphadenopathy: Swelling of the lymph nodes, referred to as lymphadenopathy, is commonly observed in Monkeypox infection. The affected lymph nodes may become enlarged, tender, and palpable.
Polymerase chain reaction method: The process begins by extracting the viral genetic material from clinical samples, such as skin lesions or respiratory secretions, and then subjecting it to PCR amplification using specific primers that target regions of the Monkeypox virus genome, the genes commonly targeted for conventional PCR testing of Monkeypox virus include hemagglutinin, the acidophilic-type inclusion body gene, and the crmB gene. These genes are specific to the Monkeypox virus and can serve as reliable markers for its detection. PCR primers designed to amplify regions within these genes can amplify and detect Monkeypox virus DNA in clinical samples. By targeting multiple genes, PCR testing enhances the sensitivity and specificity of the diagnostic assay, allowing for accurate identification of Monkeypox virus infection.
Western blot technique: The viral proteins present in the sample are separated based on their molecular weight using gel electrophoresis. The proteins are loaded onto a polyacrylamide gel and subjected to an electric field, causing them to migrate through the gel matrix. The separated proteins are transferred onto a solid membrane, typically made of nitrocellulose or polyvinylidene fluoride. After transfer, the membrane is blocked with a protein-blocking agent to prevent non-specific binding. Specific antibodies that recognize the target viral proteins are added to the membrane. If present in the sample, these primary antibodies will bind to the corresponding viral proteins. To visualize the bound antibodies, a secondary antibody is added. This secondary antibody is linked with a fluorescent dye or an enzyme. When exposed to a specific substrate, the enzyme generates a detectable signal, while the fluorescent dye emits light of a specific wavelength when excited by appropriate light. The presence of the viral proteins is indicated by bands on the membrane, which correspond to the specific target proteins. The intensity of the bands can be correlated with the amount of viral protein present in the sample.
Enzyme-linked immunosorbent assay: It is the most widely used diagnostic technique for detecting Monkeypox virus-specific antibodies in patient serum. In ELISA, the virus-specific antigens are immobilized onto a solid surface, such as a microplate, and then the patient’s serum is added. If antibodies against the Monkeypox virus are present in the serum, they react to the immobilized antigens. This binding is detected using an enzyme-linked secondary antibody that produces a colorimetric signal, indicating the presence of Monkeypox virus-specific antibodies.
Keep skin dry and uncovered (unless in a room with someone else): This practice can help reduce moisture and promote the healing of skin lesions. It may also restrict the spread of infection to others, as direct skin-to-skin contact can facilitate transmission.
Avoid touching items in shared spaces and disinfect shared spaces frequently: Monkeypox virus can survive on surfaces for a certain period. You can minimize the risk of indirect transmission by avoiding unnecessary contact with shared items and frequently disinfecting commonly touched surfaces.
Use saltwater rinses for sores in the mouth: Saltwater rinses can temporarily relieve mouth sores associated with Monkeypox virus infection. They can help cleanse the mouth, reduce inflammation, and promote healing. However, seeking medical advice to manage oral symptoms appropriately is essential.
Take sitz baths or warm baths with baking soda or Epsom salts for body sores: Soaking in sitz baths or warm baths with Epsom salts or baking soda can soothe discomfort associated with body sores. It can provide relief from itching, reduce inflammation, and promote healing.
Mpox (Monkeypox) (who.int)
Monkeypox: epidemiology, pathogenesis, treatment and prevention | Signal Transduction and Targeted Therapy (nature.com)
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