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Reports of a small outbreak of a polio-like disease in California

Discussion in 'Other Health News and Research' started by Bob, Feb 24, 2014.

  1. Bob

    Bob

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    Reports of a small outbreak of a polio-like disease in California, possibly associated with enterovirus-68.

    BBC News
    24 February 2014
    http://www.bbc.co.uk/news/health-26289614

     
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  2. beaker

    beaker ME/cfs 1986

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    I was just going to post this. My source : Physicians' Watch. Here's what they had to say (They also provided link to abstract I put at bottom):
    LInk to Abstract
     
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  3. Fuschia

    Fuschia

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  4. alex3619

    alex3619 Senior Member

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    The enteroviral theory of ME is probably one of the strongest even now. Its not discredited.

    Its long been known that enteroviruses can cause polio, at least in mice, but its not a common event.
     
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  5. Forebearance

    Forebearance Senior Member

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    This outbreak sounds scary to me.
    In the USA Today newspaper this weekend, they report that 25 cases are being investigated, all still in California.

    I wonder if this will be on the minds of the doctors and researchers who go to the IACFS conference in San Francisco in March.
     
    Last edited: Feb 25, 2014
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  6. Ecoclimber

    Ecoclimber Senior Member

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    Journal of Virology
    J Virol. 2014 Mar;88(5):2374-84. doi: 10.1128/JVI.03070-13. Epub 2013 Dec 26.
    Antigenic and Receptor Binding Properties of Enterovirus 68
    Tadatsugu Imamuraa,Michiko Okamotoa,Shin-ichi Nakakitab,Akira Suzukia,Mariko Saitoc,Raita Tamakia,Socorro Lupisang,Chandra Nath Roya,Hiroaki Hiramatsuf,Kan-etsu Sugawarad,Katsumi Mizutae,Yoko Matsuzakid,Yasuo Suzukif and Hitoshi Oshitania

    ABSTRACT
    Increased detection of enterovirus 68 (EV68) among patients with acute respiratory infections has been reported from different parts of the world in the late 2000s since its first detection in pediatric patients with lower-respiratory-tract infections in 1962.

    However, the underlying molecular mechanisms for this trend are still unknown. We therefore aimed to study the antigenicity and receptor binding properties of EV68 detected in recent years in comparison to the prototype strain of EV68, the Fermon strain. We first performed neutralization (NT) and hemagglutination inhibition (HI) tests using antisera generated for EV68 strains detected in recent years. We found that the Fermon strain had lower HI and NT titers than recently detected EV68 strains. The HI and NT titers were also significantly different between strains of different genetic lineages among recently detected EV68 strains. We further studied receptor binding specificities of EV68 strains for sialyloligosaccharides using glycan array analysis. In glycan array analysis, all tested EV68 strains showed affinity for α2-6-linked sialic acids (α2-6 SAs) compared to α2-3 SAs.

    Our study demonstrates that emergence of strains with different antigenicity is the possible reason for the increased detection of EV68 in recent years. Additionally, we found that EV68 preferably binds to α2-6 SAs, which suggests that EV68 might have affinity for the upper respiratory tract.

    IMPORTANCE:
    Numbers of cases of enterovirus 68 (EV68) infection in different parts of the world increased significantly in the late 2000s. We studied the antigenicity and receptor binding properties of recently detected EV68 strains in comparison to the prototype strain of EV68, Fermon.

    The hemagglutination inhibition (HI) and neutralization (NT) titers were significantly different between strains of different genetic lineages among recently detected EV68 strains. We further studied receptor binding specificities of EV68 strains for sialyloligosaccharides using glycan array analysis, which showed affinity for α2-6-linked sialic acids (α2-6 SAs) compared to α2-3 SAs.

    Our study suggested that the emergence of strains with different antigenicities was the possible reason for the increased detections of EV68 in recent years. Additionally, we revealed that EV68 preferably binds to α2-6 SAs. This is the first report describing the properties of EV68 receptor binding to the specific types of sialic acids.

    Human enterovirus 68 (EV68) (species, Human enterovirus D; genus, Enterovirus; family, Picornaviridae) was first isolated in the United States from pediatric patients hospitalized with lower-respiratory-tract infections in 1962 (1).

    Since its first detection, EV68 has only rarely been identified. In an enterovirus surveillance conducted in the United States from 1970 to 2005, only a total of 26 strains were reported over 35 years (2).

    However, the number of reported EV68 cases increased dramatically in the late 2000s, in different parts of the world (38). The underlying molecular mechanism for this sudden increase of EV68 detections in recent years is still unknown.....

    .....
    Considering that all EV68 strains tested showed binding specificity to α2,6-linked sialic acid terminals, EV68 might have affinity for the upper respiratory tract. However, several previous studies reported that the detection rate of EV68 was significantly higher among patients hospitalized with severe lower-respiratory-tract infections than those visiting outpatient clinics with mild upper-respiratory-tract infections (6, 8, 10). Therefore, there might be unknown mechanisms for severe infections with EV68 other than the distribution of viral receptors.

    In the species human enterovirus D (HEV-D), three serotypes, including EV68, EV70, and EV94 are known to causes illness in human (31, 32). The VP1 sequences, the most variable genome region of enteroviruses, EV68 were shown to be closely related to those of EV70 and EV94 (26, 32). It was previously reported that EV70 has affinity for α2-3 SAs (33). Although the genome regions of EV68 and EV70 associated with their affinity for SAs are still unknown, it might be possible that EV68 and EV70 share similar amino acid sequences, which are responsible for the receptor binding.

    It is well known that influenza viruses have neuraminidase (sialidase) activity, by which the newly synthesized viral proteins are removed from SAs, and the virus progenies are released from the host cell surface (34). However, in our study, we did not detect such enzymatic activities for EV68 by the MUNANA assay. Several members of the family Picornaviridae are reported to have affinity for SAs (33, 35); however, it is unknown if they have sialidase activities. It was previously shown that, in contrast to enveloped viruses, nonenveloped viruses are released from the host cells by disintegration of the cells by using mechanisms such as cell lysis (36). On the other hand, influenza viruses are enveloped viruses, and the budding of the viral progenies is dependent on the interaction between the host cell membrane and the viral proteins, including HA and NA (34). The reasons for the lack of sialidase activity in EV68 strains might lie in those differences in the virus-release mechanisms.

    In conclusion, our study showed that EV68 detected in recent outbreaks possesses highly divergent antigenicity compared to strain Fermon. The emergence of strains with different antigenicity was suggested as a possible mechanism for the recent increase in the rate of detection. However, further studies using strains detected at different time points between 1962 and 2010 are required for drawing any conclusions. Moreover, the antigenic differences were also detected among the strains of 3 genetic groups. The roles of those antigenic differences in the transmission dynamics of EV68 in the community also need to be further clarified.

    We also demonstrated that EV68 preferably binds to α2-6 SAs without sialidase activities. In the study, we did not find any differences in the receptor binding properties among the EV68 strains; therefore, the association of the receptor recognition patterns with the recent EV68 outbreaks remains elusive. Furthermore, although our findings suggested that EV68 receptors are commonly distributed in the upper respiratory tract in humans, there is epidemiological and clinical evidence suggesting that EV68 is more likely to cause severe respiratory infections. Therefore, further studies are needed to gain an overview of pathogenesis for the severe respiratory illnesses associated with EV68 infections.

    Interesting since enterovirus EV 71 is the usually associated with poliomyelitis-like paralysis
    For the full text article click on the link above:
     
    Last edited: Feb 25, 2014
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  7. lnester7

    lnester7 Seven

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    What is this coasaxie 68? I googled and couldn't find anything on it. I know I have no been tested for it I am just curious if in adults could show up in soub groups here.

    Edit: Enterovirus 68.
     
    Last edited: Feb 24, 2014
  8. alex3619

    alex3619 Senior Member

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  9. Tristen

    Tristen Senior Member

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    "Dr Waubant suspects similar cases in Asia could explain why California is affected, but not the rest of the US".

    Huh???

    20 cases within a 100 mile radius sure sounds like a cluster outbreak to me. Sounds like this is happening in the bay area......yikes.
     
  10. Dreambirdie

    Dreambirdie work in progress

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    yikes is right!
     
  11. alex3619

    alex3619 Senior Member

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    What happens in a few years? Will there be an ME incidence spike?
     
  12. SOC

    SOC Senior Member

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    I think he means that it might have been brought over from Asia to California (which has a large Asian immigrant population) by an individual or small family group. That would make the exposed group fairly confined.... for a time.
     
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  13. Sushi

    Sushi Senior Member Albuquerque

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  14. Tristen

    Tristen Senior Member

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    Don't know what's happening in Asia, but I find it curious that it's only children that are affected here (so far).
     
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  15. Bob

    Bob

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    I wonder what age the children, and how recently they received a vaccination for polio.
     
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  16. Sparrowhawk

    Sparrowhawk Senior Member

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    Good question, @Bob .
     
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  17. Dreambirdie

    Dreambirdie work in progress

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    Yes, good question.
    We'll probably never know, because of the push to have kids vaccinated.
     
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  18. Tristen

    Tristen Senior Member

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    My thoughts exactly.....but the Polio vaccine is not the only one with potential adverse effects like those seen in these kids.
     
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  19. Dreambirdie

    Dreambirdie work in progress

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  20. Dreambirdie

    Dreambirdie work in progress

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    “Polio-like” Cluster in California Has Eerie Echoes
    Great article: http://www.ageofautism.com/2014/02/polio-like-cluster-in-california-has-eerie-echoes.html

    "In that 12,000-word series, we argued that a fresh look at the evidence suggested that for millennia, polio was almost always a harmless enterovirus – a stomach bug – until late in the 19th century. That's when a new pesticide called lead arsenate allowed the virus access to the nervous system, where it reached the spinal cord; this combination was the trigger for the first outbreaks of the paralytic disease called poliomyelitis.

    “The reality, we believe, is that the virus itself was just half the epidemic equation -- necessary but not sufficient to create The Age of Polio," we wrote. "Outbreaks were not caused solely by poliovirus – the microbe was an ancient and heretofore harmless intestinal bug -- but by its interaction with a new toxin, most often innovative pesticides used to treat fruits and vegetables.” When children who were infected with the virus ate lead arsenate-laden produce, they were exquisitely vulnerable...."

    "So what’s going on with this latest “polio-like” outbreak, which the doctors in California suspect may be the result of another (non-polio) enterovirus? Who knows, but I consider it eminently reasonable to put toxins on the table when I come across the words “enterovirus,” “San Francisco,” “polio-like” and “cluster” in the same news story."
     
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