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PANDEMIC ALERT LEVEL
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Now tracking the new emerging South Africa Omicron Variant

And the next pandemic may be.....

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KiwiMum View Drop Down
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    Posted: September 30 2022 at 12:05pm

Cheerful news from the UK's Daily Mail this morning with an article highlighting what the next pandemic may be. 

It's a strain of Simian Hemorrhagic Fever that kills every single monkey that ever gets it. 

https://www.dailymail.co.uk/health/article-11266705/New-deadly-Ebola-like-virus-lives-monkeys-Africa-poised-spillover-humans.html

Those who got it wrong, for whatever reason, may feel defensive and retrench into a position that doesn’t accord with the facts.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote roni3470 Quote  Post ReplyReply Direct Link To This Post Posted: October 02 2022 at 4:57pm

well that chills me down to my very bones!!

NOW is the Season to Know

that Everything you Do

is Sacred
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Post Options Post Options   Thanks (0) Thanks(0)   Quote KiwiMum Quote  Post ReplyReply Direct Link To This Post Posted: October 02 2022 at 6:04pm

Me too!!!!!

Those who got it wrong, for whatever reason, may feel defensive and retrench into a position that doesn’t accord with the facts.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Dutch Josh Quote  Post ReplyReply Direct Link To This Post Posted: October 03 2022 at 2:35am

[url]https://en.wikipedia.org/wiki/Deltaarterivirus_hemfev[/url] or https://en.wikipedia.org/wiki/Deltaarterivirus_hemfev ;

Deltaarterivirus hemfev

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Synonyms[1]
Virus classificatione
Deltaarterivirus hemfev
(unranked):Virus
Realm:Riboviria
Kingdom:Orthornavirae
Phylum:Pisuviricota
Class:Pisoniviricetes
Order:Nidovirales
Family:Arteriviridae
Genus:Deltaarterivirus
Subgenus:Hedartevirus
Species:
Deltaarterivirus hemfev

Simian hemorrhagic fever virus

Deltaarterivirus hemfev, formerly Simian hemorrhagic fever virus or simian haemorrhagic fever virus (SHFV), is a highly pathogenic virus in monkeys. It is a positive-stranded RNA virus classified in the family Arteriviridae. It is the only member of the subgenus Hedartevirus.[2]

Hosts[edit]

Patas are believed to be the natural host for the virus since about 50% of wild patas monkeys have antibodies for the virus, while antibodies are much less prevalent in other simian species such as vervets and baboons. In macaques, however, infection with this virus can result in acute severe disease with high mortality. Recently, red colobus monkeys and red-tailed guenons have been identified as natural hosts for SHFV.[3][4]

Symptoms[edit]

Asymptomatic infection of the virus can occur in patas monkeys, vervet monkeys, and baboons, although it is observed primarily in patas monkeys. Infection has a rapid onset with animals developing a high fever, facial edemacyanosisanorexiamelena, and may begin to hemorrhage at the cutaneoussubcutaneous, and retrobulbar levels. Thrombocytopenia will develop soon after. Death usually occurs within 10–15 days after symptoms appear.[5]

DJ..so natural hosts now are detected (article missed that point...) 

[url]https://www.coronaheadsup.com/health/ebola/ebola-the-risk-of-international-spread-cannot-be-ruled/[/url] or 

https://www.coronaheadsup.com/health/ebola/ebola-the-risk-of-international-spread-cannot-be-ruled/

WHO – “The currently affected Mubende district [of Uganda] has no international borders – nevertheless, the risk of international spread cannot be ruled out due to the active cross-border population movement.”.

DJ..longer article...Some estimates put CoViD-infections worldwide at 3 billion (out of almost 8 billion people on this planet...). There are indications CoViD-infection may weaken immunity...it could be linked to Monkeypox/MPX outbreak...

Some historians claim one of the five known Roman expeditions south of the Sahara into Africa may have reached the sources of the Nile...but also did catch Ebola...(most likely a lot of those infected did not survive the journey...[url]https://en.wikipedia.org/wiki/Antonine_Plague[/url] or https://en.wikipedia.org/wiki/Antonine_Plague not related...[url]https://en.wikipedia.org/wiki/Plague_of_Cyprian[/url] or https://en.wikipedia.org/wiki/Plague_of_Cyprian ...). 

I do see [url]https://thebulletin.org/2022/09/is-the-next-pandemic-brewing-on-the-netherlands-poultry-farms/[/url] or https://thebulletin.org/2022/09/is-the-next-pandemic-brewing-on-the-netherlands-poultry-farms/ H5N1-like "bird flu" more likely as another pandemic...CoViD may stay pandemic ....(just like HIV/AIDS pandemic is not over...). 

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Dutch Josh Quote  Post ReplyReply Direct Link To This Post Posted: October 05 2022 at 2:35am

[url]https://www.cell.com/cell/fulltext/S0092-8674(22)01194-1[/url] or https://www.cell.com/cell/fulltext/S0092-8674(22)01194-1 ;

Highlights

  • SHFV uses an intracellular receptor, CD163, for cellular entry
  • CD163 divergence in primates of some species poses a barrier to SHFV entry
  • All cellular proteins required for SHFV replication are functional in human cells
  • SHFV replication in human cells suggests potential for zoonotic transmission

Summary

Simian arteriviruses are endemic in some African primates and can cause fatal hemorrhagic fevers when they cross into primate hosts of new species. We find that CD163 acts as an intracellular receptor for simian hemorrhagic fever virus (SHFV; a simian arterivirus), a rare mode of virus entry that is shared with other hemorrhagic fever-causing viruses (e.g., Ebola and Lassa viruses). Further, SHFV enters and replicates in human monocytes, indicating full functionality of all of the human cellular proteins required for viral replication. Thus, simian arteriviruses in nature may not require major adaptations to the human host. Given that at least three distinct simian arteriviruses have caused fatal infections in captive macaques after host-switching, and that humans are immunologically naive to this family of viruses, development of serology tests for human surveillance should be a priority.

Simian hemorrhagic fever is a lethal disease that has been documented in captive Asian macaques (Macaca spp.). Outbreaks have occurred in macaque colonies worldwide (Figure 1A) and have been traced to at least three different simian viruses (Figure 1B, in red) classified in subfamily Simarterivirinae (NidoviralesArteriviridae) (

). These simian arteriviruses likely entered primate facilities through the import of subclinically infected wild African monkeys. To date, primate facilities remain vigilant about preventing exposure to these viruses (

). Human infections at affected primate facilities have not been detected. Further, there is no way to surveil for prior human exposure in Africa, where these viruses are endemic in primates, because no serology tests exist. In the absence of strong biological indications that humans could be at risk of infection with these viruses, there has been little impetus to interrogate the interface between nonhuman primates and humans in Africa to exclude cryptic spillover events or subclinical infection cycles.

Although the natural primate reservoirs of these viruses remain poorly understood, recent discovery efforts have identified broad arterivirus diversity in apparently healthy African monkeys of numerous species ranging across Africa (Figure 1C) (). Infected monkeys can carry high viral loads (). In some locations, primates of these species interact with people in direct and often aggressive ways, leading to high risk of exposure for humans. For instance, red colobus monkeys in western Uganda are infected with high viral loads of two simian arteriviruses () and are known to bite and scratch local people (). Such human-primate antagonism is widespread and increasing across Africa ().
The recent finding that arteriviruses can replicate in primary ape (chimpanzee and gorilla) cells () evokes parallels to simian immunodeficiency virus (SIV; Retroviridae). SIV first crossed from African monkeys into apes, a key “stepping-stone” event that ultimately led to the evolution and emergence of the pandemic strain of HIV (HIV-1 group M) in humans (). Like arteriviruses, SIV can cause spillover infection of captive macaques (). In addition, simian arteriviruses and SIVs are both endemic in African primates (), cause long-lasting subclinical infections in their hosts (), have high mutation rates that produce diverse viral swarms (), and primarily induce fatal disease after host switching (). Thus, it is important to determine whether simian arteriviruses have the potential to infect humans (). Akin to the example of HIV-1, there is no expectation of resistance in the human population because there are no related human arteriviruses that would give humans cross-protective immunity.

See also [url]https://www.thailandmedical.news/news/breaking-u-s-nih-study-warns-of-potetial-human-outbreak-of-a-new-primate-hemorrhagic-fever-causing-arterivirus-from-africa-that-is-far-worse-than-hiv[/url] or https://www.thailandmedical.news/news/breaking-u-s-nih-study-warns-of-potetial-human-outbreak-of-a-new-primate-hemorrhagic-fever-causing-arterivirus-from-africa-that-is-far-worse-than-hiv for further discussion...

[url]https://afludiary.blogspot.com/2022/10/study-influenza-h6n6-viruses-isolated.html[/url] or https://afludiary.blogspot.com/2022/10/study-influenza-h6n6-viruses-isolated.html discussing how flu-types are developing towards a major risk (potential mix with CoViD...Flu may mobilize immunity against other infections...however CoViD may not do so...so people with CoViD may be more vulnerable for all kinds of flu...). 

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: October 05 2022 at 3:31am

Really?  Why do you like just stirring the pot!  Do you bother to check your facts about the number of mutations this virus would need to infect a human??

For example

Abstract

Hybridomas secreting monoclonal antibodies to simian virus 5 (SV5) were obtained following immunization of mice with purified preparations of a human isolate (LN) of SV5. Immune precipitation studies showed that these monoclonal antibodies had specificities for the haemagglutinin-neuraminidase (HN), fusion (F), nucleo-, matrix and phospho- (P) proteins of SV5. By use of a radioimmune competition assay the monoclonal antibodies to the HN protein were assigned to four groups, members of which recognized different antigenic sites on the protein. All the anti-HN antibodies and the anti-F antibody neutralized virus infectivity. The 54 monoclonal antibodies obtained were used to determine whether there were antigenic differences between five human, two canine and one simian isolate of SV5. Although most of the monoclonal antibodies reacted with all isolates, a few did reveal antigenic differences in the HN, F and P proteins. Furthermore, analysis by SDS-PAGE showed that while the electrophoretic mobilities of most of the virus polypeptides of these isolates were similar some differences could be detected. In particular the P protein showed the most marked mobility differences between the human, canine and simian isolates. Slight differences in the mobility of the F1 glycoprotein could also be visualized.

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: October 05 2022 at 3:46am

Try this one too

1997). Simian Virus 40 (SV40), a Possible Human Polyomavirus (Workshop Held at NIH). Emerging Infectious Diseases3(2), 245-247. https://doi.org/10.3201/eid0302.970227.

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: October 05 2022 at 3:52am

And this one

The Maximum A Posteriori relative probability of hypermutation in SFV sequences derived from monkeys (green) or humans (blue) demonstrating that human sequences are shifted to the right and therefore more likely to be hypermutated (top). The most common dinucleotide context for each sample (middle) and presence of non-sense mutations (bottom) are also shown for each sample.
Image from Matsen, et al., 2014.

Foamy viruses are a group of retroviruses that ubiquitously infect primates and some other mammals. Every examined primate except humans is infected with a simian foamy virus (SFV), and these viruses have co-speciated with their hosts for millions of years (Switzer, et al.,  2005). SFV is latent in most infected monkey cells, including blood cells, and only replicates in oral mucosa. Infectious virus is thought to be secreted into the saliva from the oral mucosa. Humans in contact with monkeys are frequently infected with SFV through contact with monkey saliva; however, the virus does not replicate efficiently in humans and there has been no documented case human-to-human SFV transmission. Thus far, there do not appear to be pathogenic consequences of SFV infection for either monkeys or humans. 

It is currently unclear why SFV does not efficiently infect humans. To understand this difference in host susceptibility, the laboratories of Lisa Jones-Engel (University of Washington), Maxine L. Linial (Basic Sciences Division) with their longstanding collaboration exploring the epidemiology and virology of SFV, teamed up with Erick Matsen’s laboratory (Public Health Sciences Division), along with an international team of collaborators, to develop a Bayesian approach to identify APOBEC-mediated hypermutation in SFV DNA. In a recent paper published in PLoS Computational Biology, Matsen, et al. demonstrate that human APOBEC3G mutates SFV and likely represents a barrier to cross-species transmission.

APOBEC3s are a family of cytidine deaminases that generate an excess of G to A mutations (hypermutation) in the viral genome during reverse transcription. Hypermutation results in nonsense and missense mutations that can prevent further viral replication by disrupting viral proteins. Individual APOBECs act on different nucleotide contexts. For example, APOBEC3G induces mutations in a GG dinucleotide context. Traditionally, Fisher’s exact test has been used to identify signatures of APOBEC3-related hypermutation. However, this statistical test is inaccurate in situations with modest rates of hypermutation, as is the case with APOBEC3. To address this and other shortcomings with the Fisher’s exact test, Matsen, et al. developed a Bayesian approach to more accurately quantify the rate of mutation within a particular APOBEC3 context relative to the rate of mutation outside this context. This approach also provides a measure of the effect size, e.g. if APOBEC3 can act in a given context what is the probability that it will mutate the sequence. Overall, this Bayesian method is more accurate than currently used methods to quantify hypermutation in a given sequence.

To determine whether APOBEC3 inhibits SFV replication in humans, Matsen et al. assayed the SFV gag gene, which encodes the viral structural proteins and is the most variable gene in SFV, for signs of hypermutation. In gag sequences derived from either free-ranging macaques or from the blood of zoonotically infected humans the team found that human-derived SFV sequences had significantly higher levels of hypermutation comparing either blood samples from the two species (p = 1.7×10-4) or comparing human blood samples to macaque buccal (p = 4.3×10-4). Furthermore, hypermutated human sequences were significantly more likely to contain stop codons in the gag coding region (p = 6.5×10-13) that would prevent viral replication.  Hypermutation in the human samples was primarily associated with either GG or GR dinucleotides, while the macaque samples were most frequently in GA or GM dinucleotide contexts, suggesting that different APOBEC3 family members may be active in the different species. Taken together, these data suggest that APOBEC3G presents a barrier to the cross-species transmission of SFV to humans.

Matsen et al. have developed a new, powerful tool to more sensitively identify signatures of hypermutation. In the current study, this Bayesian approach demonstrated that human-derived SFV sequences has undergone significant APOBEC3-mediated hypermutation, providing indirect evidence that the virus does go through at least one round of replication in humans. Going forward, "another interesting question is whether the non-structural SFV protein Bet is involved in protecting the virus from APOBEC3-mediated hypermutation," said Dr. Maxine Linial.

Matsen FA 4th, Small CT, Soliven K, Engel GA, Feeroz MM, Wang X, Craig KL, Hasan MK, Emerman M, Linial ML, Jones-Engel L. 2014. A novel bayesian method for detection of APOBEC3-mediated hypermutation and its application to zoonotic transmission of simian foamy viruses. PLoS Comput Biol doi: 10.1371/journal.pcbi.1003493.

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Dutch Josh Quote  Post ReplyReply Direct Link To This Post Posted: October 05 2022 at 4:13am

Usk, 

Thus, simian arteriviruses in nature may not require major adaptations to the human host. Given that at least three distinct simian arteriviruses have caused fatal infections in captive macaques after host-switching, and that humans are immunologically naive to this family of viruses, development of serology tests for human surveillance should be a priority.

what I make of this is humans could catch [url]https://en.wikipedia.org/wiki/Deltaarterivirus_hemfev[/url] or https://en.wikipedia.org/wiki/Deltaarterivirus_hemfev it...The fact they so far did not catch it may be in the fact most humans never will be in close contact with (infected) macaques...

But if I read that in a wrong way-please correct me !

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: October 05 2022 at 4:19am

You may not have gotten to the last nih summary. Humans have a natural antigenic shift because of our common ancestry. This makes viral jumps from primate to human very unlikely and any exposure may also be recognized by our immune system and less likely to be lethal. In other words Monkey viruses like monkey pox are recognized by our immune system.  That is my take on this. It is the non primate viruses we need to watch out for

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Dutch Josh Quote  Post ReplyReply Direct Link To This Post Posted: October 05 2022 at 10:00pm

With all respect, from the Daily Mail article;

Experts at the University of Colorado Boulder are raising the alarm due to SHFV's 'compatibility… with humans'. 

In a lab study, they found virus is able to latch on to a human receptor with ease and make copies of itself.

Senior author of the study Dr Sara Sawyer said: 'This animal virus has figured out how to gain access to human cells, multiply itself, and escape some of the important immune mechanisms we would expect to protect us from an animal virus. 


DJ..(they also refer to HIV-monkey links).but non-primate virussess (bat-corona virusses) indeed are a major worry as well...

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