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Monkeypox is a disease caused by the monkeypox virus. It spreads through close, personal, often skin-to-skin contact.
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Cases as of November 17, 2022
Confirmed cases in BC: 183Health authorities with cases:
Epidemiologicaldata are summarized to provide an understanding of the population(s) affected by monkeypox transmission and potential exposures to support the response.
B.C. is working closely with federal and provincial partners to stop the spread of monkeypox.
While most, but not all, recent global infections are among men who identify as gay, bisexual, or other men who have sex with other men, the virus can affect anyone through close person-to-person contact. Most cases in the current outbreak have occurred from close, intimate contact during sex. The risk to the general population in B.C. is considered low.
We will update this information as we learn more about the current outbreak.
Monkeypox can spread from animals to humans, from person to person and through contact with objects that have been used by someone with monkeypox.
Monkeypox spreads through close, personal, often skin-to-skin contact, including through:
Most cases in the current outbreak have been passed from person to person during close, intimate contact during sex.
Monkeypox can present in different ways. Most people experience symptoms thatlast 2 to 4 weeks and occur in two stages.
In the first stage, symptoms can include:
The second stage usually starts 1 to 5 days after the first stage.
In the second stage, a rash (sores/blisters) develops.
Some people experience symptoms differently. For example:
some may experience first stage symptoms after the appearance of sores
some can have a small number of sores on one or a few body parts, sometimes only in the mouth or genital areas.
Image credit: United Kingdom
Public health is reaching out to known contacts of the cases at risk of developing the infection.
Please note: Public health does not use pre-recorded or automated calls to notify individuals of infections or possibleexposure to monkeypox or other communicable diseases. If you receive one of these scam calls, do not engage and do notprovide personal information over the phone.
If monkeypox is confirmed, public health will contact you to give more instructions. Monkeypox is usually a mild illness and most people recover on their own after a few weeks. However, some people may experience moderate or severe disease, and will need to see their healthcare provider. People experiencing more severe disease may require medications to manage pain or skin infections, or in rare cases, need other supportive treatment in hospital.
Please see your healthcare provider or go to your nearest Urgent Primary Care Centre or Emergency Department if you experience the following after testing positive for monkeypox:
There are no well-established treatments for monkeypox. Antiviral medication may be considered on a case-by-case basis.
A supply of vaccine that protects against monkeypox has been made available to BC by the federal government and vaccination has been offered to at-risk populations since June 2022. The vaccine, called IMVAMUNE, is given in a series of two doses given 28 or more days apart. It can be given following a recognized exposure to infection (ideally within 4 days) to provide protection against monkeypox, or can be given in advance of an exposure. It helps your body build immunity.
People who are eligible can now book first or second dose appointments.
Eligibility for the vaccine in BC has been guided by information about people who have acquired this infection. Should the characteristics of these people change as transmission continues to occur, the eligibility may be adjusted accordingly.
Use of this vaccine to control the outbreak of monkeypox in BC has been successful in bringing cases to a low number. As of October 2022, small numbers of infections continue to occur each week among unvaccinated eligible individuals which is why they continue to be encouraged to get vaccinated.
The vaccine can be used two ways
Two-Spirit and transgender people andcisgender males whoself-identify as belonging to the gay, bisexual and other men who have sex with men community.
The vaccine is not available to individuals of any gender who are not part of the community of gay, bisexual and other men who have sex men, unless they have been identified as a close contact of a confirmed case.
Misidentifying oneself as eligible for monkeypox vaccine directs this critical tool away from people most at risk, and limits its utility in preventing onward transmission, and from protecting the wider population from a bigger outbreak.
Due to limited supply, this vaccine is intended for residents of Canada or those visiting B.C. for prolonged periods of time. People from outside Canada should not travel to B.C.vaccine clinics for immunization; we cannot provide the vaccine to those visiting the province for the purpose of being vaccinated. Please contact your local Public Health unit for information about receiving monkeypox vaccine.
Imvamune is given in a series of two doses. You must wait at least 28 days after your first dose to get your second dose.
Subcutaneous or intradermal injection
To ensure there is enough vaccine to offer second doses to all who are eligible, a second dose will be offered one of two ways: subcutaneous injection or intradermal injection.
To learn more about vaccinations, eligibility criteriaand to book an appointment, refer toyour region:
Appointments are added regularly. If there are no available appointments, please check back.
This document provides suggestions for event organizers, business owners, community organizations and leaders to help prevent spread as people gather to celebrate during the Pride festival season. It includes information about:
Learn more: Monkeypox Guidance for Events during Pride Festival Season
Most of the recent monkeypox cases are happening through close contacts between men who identify as having sex with other men.
Stigmatizing people because of a disease is never okay. Anyone can get or pass on monkeypox, regardless of their sexuality.
Be aware of the monkeypox situation in the places you visit and take the same precautions you would use at home. Some people have been exposed or got monkeypox from close contact during sexual activity while travelling.
Domestic travel
International travel
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Species of virus
Influenza A virus (IAV) causes influenza in birds and some mammals, and is the only species of the genus Alphainfluenzavirus of the virus family Orthomyxoviridae.[1] Strains of all subtypes of influenza A virus have been isolated from wild birds, although disease is uncommon. Some isolates of influenza A virus cause severe disease both in domestic poultry and, rarely, in humans.[2] Occasionally, viruses are transmitted from wild aquatic birds to domestic poultry, and this may cause an outbreak or give rise to human influenza pandemics.[3][4]
Influenza A viruses are negative-sense, single-stranded, segmented RNA viruses. The several subtypes are labeled according to an H number (for the type of hemagglutinin) and an N number (for the type of neuraminidase). There are 18 different known H antigens (H1 to H18) and 11 different known N antigens (N1 to N11).[5][6] H17N10 was isolated from fruit bats in 2012.[7][8] H18N11 was discovered in a Peruvian bat in 2013.[6]
Each virus subtype has mutated into a variety of strains with differing pathogenic profiles; some are pathogenic for one species but not others, some are pathogenic to multiple species.
A filtered and purified influenza A vaccine for humans has been developed and many countries have stockpiled it to allow a quick administration to the population in the event of an avian influenza pandemic. Avian influenza is sometimes called avian flu, and colloquially, bird flu. In 2011, researchers reported the discovery of an antibody effective against all types of the influenza A virus.[9]
Influenza type A viruses are RNA viruses categorized into subtypes based on the type of two proteins on the surface of the viral envelope:
The hemagglutinin is central to the virus's recognizing and binding to target cells, and also to its then infecting the cell with its RNA. The neuraminidase, on the other hand, is critical for the subsequent release of the daughter virus particles created within the infected cell so they can spread to other cells.
Different influenza viruses encode for different hemagglutinin and neuraminidase proteins. For example, the H5N1 virus designates an influenza A subtype that has a type 5 hemagglutinin (H) protein and a type 1 neuraminidase (N) protein. There are 18 known types of hemagglutinin and 11 known types of neuraminidase, so, in theory, 198 different combinations of these proteins are possible.[5][6]
Some variants are identified and named according to the isolate they resemble, thus are presumed to share lineage (example Fujian flu virus-like); according to their typical host (example human flu virus); according to their subtype (example H3N2); and according to their deadliness (example LP, low pathogenic). So a flu from a virus similar to the isolate A/Fujian/411/2002(H3N2) is called Fujian flu, human flu, and H3N2 flu.
Variants are sometimes named according to the species (host) in which the strain is endemic or to which it is adapted. The main variants named using this convention are:
Variants have also sometimes been named according to their deadliness in poultry, especially chickens:
Most known strains are extinct strains. For example, the annual flu subtype H3N2 no longer contains the strain that caused the Hong Kong flu.
The annual flu (also called "seasonal flu" or "human flu") in the US "results in approximately 36,000 deaths and more than 200,000 hospitalizations each year. In addition to this human toll, influenza is annually responsible for a total cost of over $10 billion in the U.S."[10] Globally the toll of influenza virus is estimated at 290,000645,000 deaths annually, exceeding previous estimates.[11]
The annually updated, trivalent influenza vaccine consists of hemagglutinin (HA) surface glycoprotein components from influenza H3N2, H1N1, and B influenza viruses.[12]
Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 has increased from 1% in 1994 to 12% in 2003 to 91% in 2005.
"Contemporary human H3N2 influenza viruses are now endemic in pigs in southern China and can reassort with avian H5N1 viruses in this intermediate host."[13]
FI6, an antibody that targets the hemagglutinin protein, was discovered in 2011. FI6 is the only known antibody effective against all 16 subtypes of the influenza A virus.[14][15][16]
Influenza type A viruses are very similar in structure to influenza viruses types B, C, and D.[19] The virus particle (also called the virion) is 80120 nanometers in diameter such that the smallest virions adopt an elliptical shape.[20][18] The length of each particle varies considerably, owing to the fact that influenza is pleomorphic, and can be in excess of many tens of micrometers, producing filamentous virions.[21] Confusion about the nature of influenza virus pleomorphy stems from the observation that lab adapted strains typically lose the ability to form filaments[22] and that these lab adapted strains were the first to be visualized by electron microscopy.[23] Despite these varied shapes, the virions of all influenza type A viruses are similar in composition. They are all made up of a viral envelope containing two main types of proteins, wrapped around a central core.[24]
The two large proteins found on the outside of viral particles are hemagglutinin (HA) and neuraminidase (NA). HA is a protein that mediates binding of the virion to target cells and entry of the viral genome into the target cell. NA is involved in release from the abundant non-productive attachment sites present in mucus[25] as well as the release of progeny virions from infected cells.[26] These proteins are usually the targets for antiviral drugs.[27] Furthermore, they are also the antigen proteins to which a host's antibodies can bind and trigger an immune response. Influenza type A viruses are categorized into subtypes based on the type of these two proteins on the surface of the viral envelope. There are 16 subtypes of HA and 9 subtypes of NA known, but only H 1, 2 and 3, and N 1 and 2 are commonly found in humans.[28]
The central core of a virion contains the viral genome and other viral proteins that package and protect the genetic material. Unlike the genomes of most organisms (including humans, animals, plants, and bacteria) which are made up of double-stranded DNA, many viral genomes are made up of a different, single-stranded nucleic acid called RNA. Unusually for a virus, though, the influenza type A virus genome is not a single piece of RNA; instead, it consists of segmented pieces of negative-sense RNA, each piece containing either one or two genes which code for a gene product (protein).[24] The term negative-sense RNA just implies that the RNA genome cannot be translated into protein directly; it must first be transcribed to positive-sense RNA before it can be translated into protein products. The segmented nature of the genome allows for the exchange of entire genes between different viral strains.[24]
The entire Influenza A virus genome is 13,588 bases long and is contained on eight RNA segments that code for at least 10 but up to 14 proteins, depending on the strain. The relevance or presence of alternate gene products can vary:[29]
The RNA segments of the viral genome have complementary base sequences at the terminal ends, allowing them to bond to each other with hydrogen bonds.[26] Transcription of the viral (-) sense genome (vRNA) can only proceed after the PB2 protein binds to host capped RNAs, allowing for the PA subunit to cleave several nucleotides after the cap. This host-derived cap and accompanied nucleotides serve as the primer for viral transcription initiation. Transcription proceeds along the vRNA until a stretch of several uracil bases is reached, initiating a 'stuttering' whereby the nascent viral mRNA is poly-adenylated, producing a mature transcript for nuclear export and translation by host machinery.[31]
The RNA synthesis takes place in the cell nucleus, while the synthesis of proteins takes place in the cytoplasm. Once the viral proteins are assembled into virions, the assembled virions leave the nucleus and migrate towards the cell membrane.[32] The host cell membrane has patches of viral transmembrane proteins (HA, NA, and M2) and an underlying layer of the M1 protein which assist the assembled virions to budding through the membrane, releasing finished enveloped viruses into the extracellular fluid.[32]
The subtypes of influenza A virus are estimated to have diverged 2,000 years ago. Influenza viruses A and B are estimated to have diverged from a single ancestor around 4,000 years ago, while the ancestor of influenza viruses A and B and the ancestor of influenza virus C are estimated to have diverged from a common ancestor around 8,000 years ago.[33]
Influenza virus is able to undergo multiplicity reactivation after inactivation by UV radiation,[34][35] or by ionizing radiation.[36] If any of the eight RNA strands that make up the genome contains damage that prevents replication or expression of an essential gene, the virus is not viable when it alone infects a cell (a single infection). However, when two or more damaged viruses infect the same cell (multiple infection), viable progeny viruses can be produced provided each of the eight genomic segments is present in at least one undamaged copy. That is, multiplicity reactivation can occur.
Upon infection, influenza virus induces a host response involving increased production of reactive oxygen species, and this can damage the virus genome.[37] If, under natural conditions, virus survival is ordinarily vulnerable to the challenge of oxidative damage, then multiplicity reactivation is likely selectively advantageous as a kind of genomic repair process. It has been suggested that multiplicity reactivation involving segmented RNA genomes may be similar to the earliest evolved form of sexual interaction in the RNA world that likely preceded the DNA world.[38] (Also see RNA world hypothesis.)
"Human influenza virus" usually refers to those subtypes that spread widely among humans. H1N1, H1N2, and H3N2 are the only known influenza A virus subtypes currently circulating among humans.[39]
Genetic factors in distinguishing between "human flu viruses" and "avian influenza viruses" include:
Human flu symptoms usually include fever, cough, sore throat, muscle aches, conjunctivitis and, in severe cases, breathing problems and pneumonia that may be fatal. The severity of the infection will depend in large part on the state of the infected person's immune system and if the victim has been exposed to the strain before, and is therefore partially immune. Follow-up studies on the impact of statins on influenza virus replication show that pre-treatment of cells with atorvastatin suppresses virus growth in culture.[40]
Highly pathogenic H5N1 avian influenza in a human is far worse, killing 50% of humans who catch it. In one case, a boy with H5N1 experienced diarrhea followed rapidly by a coma without developing respiratory or flu-like symptoms.[41]
The influenza A virus subtypes that have been confirmed in humans, ordered by the number of known human pandemic deaths, are:
H10N3
In May 2021, in Zhenjiang, China H10N3 was reported for the first time in humans. One person was infected.[63]
According to Jeffery Taubenberger:
Researchers from the National Institutes of Health used data from the Influenza Genome Sequencing Project and concluded that during the ten-year period examined, most of the time the hemagglutinin gene in H3N2 showed no significant excess of mutations in the antigenic regions while an increasing variety of strains accumulated. This resulted in one of the variants eventually achieving higher fitness, becoming dominant, and in a brief interval of rapid evolution, rapidly sweeping through the population and eliminating most other variants.[65]
In the short-term evolution of influenza A virus, a 2006 study found that stochastic, or random, processes are key factors.[66] Influenza A virus HA antigenic evolution appears to be characterized more by punctuated, sporadic jumps as opposed to a constant rate of antigenic change.[67] Using phylogenetic analysis of 413 complete genomes of human influenza A viruses that were collected throughout the state of New York, the authors of Nelson et al. 2006 were able to show that genetic diversity, and not antigenic drift, shaped the short-term evolution of influenza A via random migration and reassortment. The evolution of these viruses is dominated more by the random importation of genetically different viral strains from other geographic locations and less by natural selection. Within a given season, adaptive evolution is infrequent and had an overall weak effect as evidenced from the data gathered from the 413 genomes. Phylogenetic analysis revealed the different strains were derived from newly imported genetic material as opposed to isolates that had been circulating in New York in previous seasons. Therefore, the gene flow in and out of this population, and not natural selection, was more important in the short term.
Fowl act as natural asymptomatic carriers of influenza A viruses. Prior to the current[when?] H5N1 epizootic, strains of influenza A virus had been demonstrated to be transmitted from wildfowl to only birds, pigs, horses, seals, whales and humans; and only between humans and pigs and between humans and domestic fowl; and not other pathways such as domestic fowl to horse.[68]
Wild aquatic birds are the natural hosts for a large variety of influenza A viruses. Occasionally, viruses are transmitted from these birds to other species and may then cause devastating outbreaks in domestic poultry or give rise to human influenza pandemics.[3][4]
H5N1 has been shown to be transmitted to tigers, leopards, and domestic cats that were fed uncooked domestic fowl (chickens) with the virus. H3N8 viruses from horses have crossed over and caused outbreaks in dogs. Laboratory mice have been infected successfully with a variety of avian flu genotypes.[69]
Influenza A viruses spread in the air and in manure, and survives longer in cold weather. They can also be transmitted by contaminated feed, water, equipment, and clothing; however, there is no evidence the virus can survive in well-cooked meat. Symptoms in animals vary, but virulent strains can cause death within a few days. Avian influenza viruses that the World Organisation for Animal Health and others test for to control poultry disease include H5N1, H7N2, H1N7, H7N3, H13N6, H5N9, H11N6, H3N8, H9N2, H5N2, H4N8, H10N7, H2N2, H8N4, H14N5, H6N5, and H12N5.
*Outbreaks with significant spread to numerous farms, resulting in great economic losses. Most other outbreaks involved little or no spread from the initially infected farms.
More than 400 harbor seal deaths were recorded in New England between December 1979 and October 1980, from acute pneumonia caused by the influenza virus, A/Seal/Mass/1/180 (H7N7).[71]
Influenza A virus has the following subtypes:
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