Sinikielitaudista, joka on Tanskassa uutta tautia eläimillä ja leviämässä Ruotsin suuntaan.Suomi vielätautivapaa.

 https://mmm.fi/-/ahvenanmaalla-saa-rokottaa-elaimia-sinikielitautia-vastaan

Sitaatti:

Maa- ja metsätalousministeriö on päättänyt kumota kiellon rokottaa eläimiä märehtijöiden sinikielitautia vastaan Ahvenanmaan maakunnan alueella. Muutos rokotuskieltoon tehtiin maa- ja metsätalousministeriön asetuksella, joka tulee voimaan 27. kesäkuuta.

Päätöksen tarkoituksena on suojata Ahvenanmaan naudat ja lampaat sinikielitautia vastaan. Sinikielitauti on polttiaisten välityksellä leviävä virustauti, jonka eri serotyyppejä esiintyy yleisesti Välimeren alueen maissa.

Uusi serotyyppi 3 on levinnyt Pohjois-Euroopassa vuodesta 2023 alkaen ja saavutti Etelä-Ruotsin syksyllä 2024. Taudin pelätään leviävän Ruotsissa edelleen kesän aikana ja mahdollisesti saapuvan Ahvenanmaalle syksyllä. Polttiaiset voivat kulkeutua tuulen mukana satoja kilometrejä. 

Rokottaminen päätettiin sallia, vaikka tautia ei vielä esiinny Ahvenanmaalla. Halutaan varmistaa, että eläimillä on rokotuksesta saatu vastustuskyky siinä vaiheessa, kun tauti mahdollisesti saapuu Ahvenanmaalle. Rokottamisen jälkeen kuluu vähintään kuusi viikkoa vastustuskyvyn saavuttamiseksi.

Euroopan komissio on hyväksynyt Suomen sinikielitaudista vapaaksi jäsenvaltioksi. Tämän aseman ansiosta märehtijöiden ja kamelieläinten tuontia rajoitetaan alueilta, joilla sinikielitautia esiintyy. Tautivapauden ylläpitämiseksi ja tartunnan varhaiseksi havaitsemiseksi eläinten rokotus sinikielitautia vastaan on ollut kiellettyä tähän asti koko Suomen alueella ja on edelleen kiellettyä muualla kuin Ahvenanmaalla. 

Suomi säilyttää tautivapaan asemansa rokotusten sallimisesta huolimatta, koska tautiseurantaa tehostetaan Ahvenanmaalla ja lähialueilla. 

Rokotus on vapaaehtoista. Eläimen omistaja tilaa rokotuksen eläinlääkäriltä, joka huolehtii rokotuksesta. Eläimen omistaja maksaa rokotteet ja rokotustyön. 
Suomessa on myyntilupa kolmelle sinikielitautirokotteelle. Kahden rokotteen kohde-eläinlajina on nauta ja lammas. Kolmannen rokotteen kohde-eläinlajina on lammas.

Sinikielitauti on märehtijöiden ja kamelieläinten virustauti, jota esiintyy useimmissa Euroopan maissa Suomea, Baltian maita ja Irlantia lukuun ottamatta. Tauti aiheuttaa eläimissä mm. sierainvuotoa, turvotusta ja kuumetta. Lampailla oireet ovat voimakkaampia ja voivat johtaa eläimen kuolemaan.

Tauti voi siirtyä emästä sikiöön ja aiheuttaa luomista tai epämuodostuneita vasikoita tai karitsoita, jos eläin saa tartunnan tiineyden alkuvaiheessa. Lypsylehmillä tauti voi aiheuttaa maidontuotannon laskua. Koska tartunta leviää polttiaisten välityksellä, eläimiä on vaikeaa suojata tartunnalta muulla tavoin kuin rokottamalla. Eläimiä rokotetaan yleisesti sinikielitautia vastaan muissa Euroopan maissa, mm. Ruotsissa. Tauti tai rokotus ei ole riski kuluttajalle ja elintarvikkeita voi myydä ja käyttää ilman rajoituksia. Sinikielitauti ei tartu ihmiseen. 

Asetuksella sallitaan myös eläinten rokotus koko Suomen alueella tutkimushankkeiden yhteydessä. Tämän muutoksen tarkoituksena on mahdollistaa porojen kokeellinen rokotus sinikielitautia vastaan. Tauti ei leviä rokotusten välityksellä. Sinikielitauti tarttuu kaikkiin märehtijöihin ja on mahdollista, että sinikielitauti leviää tulevaisuudessa polttiaisten mukana myös poronhoitoalueelle. 

 Haku: Ruminantia, Blåtungasjuka 

Vastaus: Svar på svenska

 Blåtunga är en virussjukdom som drabbar idisslare som nötkreatur och får, och sprids via svidknott. I Sverige påvisades sjukdomen för första gången på 15 år i september 2024, med spridning längs västkusten och inåt landet. Symptomen kan variera men kan inkludera feber, sår i mun och nos, dreglande, hälta och minskad mjölkproduktion. 

 

Haku suomeksi: Polttiainen (pistävä mäkäräinen)

https://fi.wikipedia.org/wiki/Polttiaiset 

Polttiaiset (Ceratopogonidae) on hyönteisten heimo. Polttiaiset ovat pienikokoisia, ja jotkin lajit imevät verta ihmisestä ja muista eläimistä, jopa toisista hyönteisistä.

Tuntomerkit

Polttiaiset muistuttavat ulkonäöltään surviaissääskiä. Aikuinen polttiainen on noin 1–1,5 millimetriä pitkä. Useimmilla polttiaislajeilla on kirjavat siivet. Koirailla on tuntosarvissaan paljon pitkiä karvoja, naarailla selvästi vähemmän. Polttiaisen pää on alaviistoon ja eturuumis työntyy sen päälle, jolloin hyönteinen näyttää kyttyräselältä. Silmät kiertävät lähes koko pään ympäri ja koskettavat päälaella toisiaan.^[2]

 Ruotsin svidknott:

 https://sv.wikipedia.org/wiki/Svidknott

 

 https://fi.wikipedia.org/wiki/Orbivirukset

 

Miksi H5N1 pandemiaa tulisi koettaa viivytellä ja ehkäistä?

 Katson uusinta tietoa  ensin.

Novel Epidemiologic Features of High Pathogenicity Avian Influenza Virus A H5N1 2.3.3.4b Panzootic: A Review.

Sacristán C, Ewbank AC, Ibáñez Porras P, Pérez-Ramírez E, de la Torre A, Briones V, Iglesias I. Transbound Emerg Dis. 2024 Sep 27;2024:5322378. doi: 10.1155/2024/5322378. eCollection 2024. PMID: 40303080 Free PMC article. Review.

The number and diversity of mammal species infected by H5N1 2.3.4.4b is unprecedented. Although considered low, this strain's potential to spillover to humans should not be underestimated, especially considering the current extremely high viral circulation in …

Avian influenza is one of the most devastating avian diseases. The current high pathogenicity avian influenza (HPAI) A virus H5N1 clade 2.3.4.4b epizootic began in the 2020-2021 season, and has caused a panzootic, considered one of the worst ever reported. The present panzootic has novel epidemiological features that represent a challenge for its prevention and control. This review examines key epidemiological changes of the disease such as seasonality, geographic spread, and host range. The seasonality of the virus has changed, and contrary to previous avian influenza epizootics, this subclade was able to persist during boreal summer. Its geographic range has expanded, with reports in all continents except Australia. During this epizootic, HPAIV H5N1 has broadened its host range, infecting hundreds of bird species, and causing the death of thousands of wild birds and over 300 million poultry. The number and diversity of mammal species infected by H5N1 2.3.4.4b is unprecedented. Although considered low, this strain's potential to spillover to humans should not be underestimated, especially considering the current extremely high viral circulation in animals and increasing adaptation to mammals. Overall, HPAI A(H5N1) clade 2.3.4.4b represents an ongoing and growing threat to poultry, wildlife, and human health.

Keywords: birds; conservation; emerging disease; epidemiology; influenza; mammals; wildlife; zoonosis.

 2.

 Ocular infectivity and replication of a clade 2.3.4.4b A(H5N1) influenza virus associated with human conjunctivitis in a dairy farm worker in the USA: an in-vitro and ferret study.

Belser JA, Pulit-Penaloza JA, Brock N, Sun X, Kieran TJ, Pappas C, Zeng H, Vu MN, Lakdawala SS, Tumpey TM, Maines TR. Lancet Microbe. 2025 Mar 17:101070. doi: 10.1016/j.lanmic.2024.101070. Online ahead of print. PMID: 40112840 Free article.

METHODS: Primary human nasal and corneal tissue constructs were infected with A(H5N1) A/Texas/37/2024 (Texas/37), A(H1N1)pdm09 A/Nebraska/14/2019 (Neb/14), and A(H7N7) A/Netherlands/219/2003 (NL/219) viruses (multiplicity of infection [MOI] of 0.01-0.0 … 

3. 

• 2009 Jun 15;48(12):1639-46.

doi: 10.1086/599031.

Clinical features of human influenza A (H5N1) infection in Vietnam: 2004-2006

Nguyen Thanh Liem  ¹ , et al.

 

4.

A H5N1  infektion yhteydessä voi esiintyä HLH-L, muta se ei kaiketi ole mikään sääntö vaan  joillakin  esiintyvä taudinkulku.   Esimerkki infektioista, joissa sitä  on ilmentynyt aiemmin.

 

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. 2012 Oct;16(10):1324-37.

Secondary hemophagocytic lymphohistiocytosis in zoonoses. A systematic review

A Cascio  ¹ , L M Pernice, G Barberi, D Delfino, C Biondo, C Beninati, G Mancuso, A J Rodriguez-Morales, C Iaria

AffiliationsPMID: 23104648

Free article

Abstract

Background: Hemophagocytic lymphohistiocytosis (HLH) is a rare syndrome that is often fatal despite treatment. It is caused by a dysregulation in natural killer T-cell function, resulting in activation and proliferation of histiocytes with uncontrolled hemophagocytosis and cytokines overproduction. The syndrome is characterized by fever, hepatosplenomegaly, cytopenias, liver dysfunction, and hyperferritinemia. HLH can be either primary, with a genetic aetiology, or secondary, associated with malignancies, autoimmune diseases, or infections.

Aim: To focus on secondary HLH complicating zoonotic diseases.

Materials and methods: PubMed search of human cases of HLH occurring during zoonotic diseases was performed combining the terms (haemophagocytic or haemophagocytosis or hemophagocytosis or hemophagocytic or erythrophagocytosis or macrophage activation syndrome) with each one of the etiological agents of zoonoses.

Results: Among bacterial diseases, most papers reported cases occurring during brucellosis, rickettsial diseases and Q fever. Regarding viral diseases, most of the cases were reported in patients with avian influenza A subtype H5N1. Among the protozoan zoonoses, most of the cases were reported in patients with visceral leishmaniasis. Regarding zoonotic fungi, most of the cases were reported in AIDS patient with histoplasmosis. No cases of secondary HLH were reported in patient with zoonotic helminthes.

Conclusions: Zoonotic diseases are an important cause of HLH. Secondary HLH can delay the correct diagnosis of the zoonotic disease, and can contribute to an adverse outcome.

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 A H5N1 pandemiana  on ennalta arvaamaton.  Kananpoikien mortaliteetti on  100%, Emme kuitenkaan ole  lintuja, joten prosentti on alle 100.  Sosioeknomiset ja yhteiskunnalliset muut  seikat voivat tietysti  nostaa mortaliteettia ihmiskunnassa. Sotakin tappaa lisäksi eivätkä ne näytä  päättyvän.  Lisäksi tuhotaan  tutkimuslaitoksia,jotka ehkäisevät pandemioita ja hoitavat   hengenvaarassa olevia. 

 

Suomen asenne A H5N1-viruksen esiintymiseen epätavallisissa lajeissa kuten lämminveriset turkiseläimet.

 https://wahis.woah.org/#/in-review/5119

SOURCE OF EVENT OR ORIGIN OF INFECTION

• Unknown or inconclusive

EPIDEMIOLOGICAL COMMENTS

Note: previously published precise location data of the outbreaks was changed to approximate in follow-up report 3 to insure privacy of the farmers. Follow-up report on 24.8.2023: Several HPAI H5N1 outbreaks on fur farms raising arctic foxes, silver foxes, American minks and raccoon dogs have been detected. Wild birds are currently considered the most likely source of the infection, based on epidemiological investigations and sequencing of the viruses. The competent authority has imposed restrictive orders on infected fur animal farms. All minks from the infected farms are culled. Other fur animals from infected farms are culled based on the decisions that are made on a case-by-case basis and do not necessarily apply to all animals on the farm. In addition, samples are taken from infected farms to monitor the course of the epidemic. If the virus is detected, the culling will continue. Veterinary authorities are working in tight collaboration with the public health authority. Improved biosecurity measures and use of personal protection equipment on fur farms are encouraged. Follow-up report on 5.10.2023: Starting from 11 September 2023, a new culling policy has been adopted and all animals on HPAI virus-positive farms, including foxes and common raccoon dogs, are culled.

 Wahis raportoi 25.4.2024  Suomessa  kasseerattujen  turkisfarmieläinten määräksi 457 232.

A H5N1 viruses, clade 2.3.4.4b

 

Review

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• 
  
• 
  

. 2025 Jun 17;99(6):e0042425.

doi: 10.1128/jvi.00424-25. Epub 2025 May 9.

Clade 2.3.4.4b highly pathogenic avian influenza H5N1 viruses: knowns, unknowns, and challenges

Zimin Xie ^{#  1   2} , Jiayun Yang ^{#  3} , Wanlin Jiao  ^{1   2} , Xueqing Li  ^{1   2} , Munir Iqbal  ³ , Ming Liao  ^{1   2} , Manman Dai  ^{1   2}

Affiliations

• PMID: 40340397
• PMCID: PMC12172449
• DOI: 10.1128/jvi.00424-25

Abstract

Since 2020, the clade 2.3.4.4b highly pathogenic avian influenza (HPAI) H5N1 viruses have caused unprecedented outbreaks in wild birds and domestic poultry globally, resulting in significant ecological damage and economic losses due to the disease and enforced stamp-out control. In addition to the avian hosts, the H5N1 viruses have expanded their host range to infect many mammalian species, potentially increasing the zoonotic risk. Here, we review the current knowns and unknowns of clade 2.3.4.4b HPAI H5N1 viruses, and we highlight common challenges in prevention. By integrating our knowledge of viral evolution and ecology, we aim to identify discrepancies and knowledge gaps for a more comprehensive understanding of the virus. Ultimately, this review will serve as a theoretical foundation for researchers involved in related avian influenza virus studies, aiding in improved control and prevention of H5N1 viruses.

Keywords: Clade 2.3.4.4b; H5N1; evolution; highly pathogenic avian influenza; pathogenicity.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

A H5N1 viruksen yksityiskohdista. vRNP-M1-NEP tumasta ulos kuljettava kompleksi

 

•  2014 Jul 18;289(29):20067-77.

doi: 10.1074/jbc.M114.569178. Epub 2014 Jun 2.The nuclear export protein of H5N1 influenza A viruses recruits Matrix 1 (M1) protein to the viral ribonucleoprotein to mediate nuclear export

Linda Brunotte  ¹ , Joe Flies  ¹ , Hardin Bolte  ¹ , Peter Reuther  ¹ , Frank Vreede  ² , Martin Schwemmle  ³

Affiliations

• PMID: 24891509
• PMCID: PMC4106323
• DOI: 10.1074/jbc.M114.569178

Abstract

In influenza A virus-infected cells, replication and transcription of the viral genome occurs in the nucleus. To be packaged into viral particles at the plasma membrane, encapsidated viral genomes must be exported from the nucleus. Intriguingly, the nuclear export protein (NEP) is involved in both processes. Although NEP stimulates viral RNA synthesis by binding to the viral polymerase, its function during nuclear export implicates interaction with viral ribonucleoprotein (vRNP)-associated M1. The observation that both interactions are mediated by the C-terminal moiety of NEP raised the question whether these two features of NEP are linked functionally. Here we provide evidence that the interaction between M1 and the vRNP depends on the NEP C terminus and its polymerase activity-enhancing property for the nuclear export of vRNPs. This suggests that these features of NEP are linked functionally. Furthermore, our data suggest that the N-terminal domain of NEP interferes with the stability of the vRNP-M1-NEP nuclear export complex, probably mediated by its highly flexible intramolecular interaction with the NEP C terminus. On the basis of our data, we propose a new model for the assembly of the nuclear export complex of Influenza A vRNPs.

Keywords: Influenza Virus; Protein Export; Ribonucleoprotein (RNP); Viral Polymerase; Viral Protein.

© 2014 by The American Society for Biochemistry and Molecular Biology, Inc. 

 

See this image and copyright information in PMC

FIGURE 1.

Schematic of the nuclear export complex. A, in the currently proposed daisy chain model of the nuclear export model, M1 interacts with the vRNP. NEP binds with its C-terminal (C) domain to vRNP-associated M1 and, with its NES-containing N terminus (N), establishes an interaction with the cellular export protein CRM1. B, refined model of the vRNP nuclear export complex. NEP interacts with the viral polymerase to provide additional binding site and support M1/vRNP association. The N-Terminus of NEP is flexible and interacts with CRM1.

Influenssatilanteesta 2025 PubMed uutinen

 Editorial: The 2025 World Health Assembly Pandemic Agreement and the 2024 Amendments to the International Health Regulations Combine for Pandemic Preparedness and Response.

Parums DV. Med Sci Monit. 2025 Jul 1;31:e950411. doi: 10.12659/MSM.950411. PMID: 40589223Abstract

The importance of pandemic preparedness is underscored by two recent and significant findings in the US, including outbreaks of measles in children and adults, as well as the demonstration of airborne transmission of the influenza A(H5N1) virus (bird flu). 

On June 1, 2024, the 77th World Health Assembly of the World Health Organization (WHO) reached a consensus on amendments to the 2005 International Health Regulations, representing a new universal legal framework for global health, pandemic preparedness, and response that will enter into force in September 2025. 

On May 20, 2025, the 78th World Health Assembly of the WHO adopted the Pandemic Agreement, following three years of negotiations that identified gaps and inequities in the global response to the COVID-19 pandemic.

 The WHO Pandemic Agreement document outlines the principles, approaches, and tools to enhance international coordination for pandemic prevention, preparedness, and response, including equitable access to vaccines, diagnostics, and therapeutics. This editorial aims to highlight the timeliness of the 2025 WHO Pandemic Agreement and the 2024 amendments to the International Health Regulations, as well as the need for improved pandemic preparedness and response at this time.

Influenssaviruksen RNP ja riippuvaisuus sinkistä hakusanana. 2 vastausta vuosilta 2004 ja 2002.

 

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Introduction of a temperature-sensitive phenotype into influenza A/WSN/33 virus by altering the basic amino acid domain of influenza virus matrix protein.

Liu T, Ye Z. J Virol. 2004 Sep;78(18):9585-91. doi: 10.1128/JVI.78.18.9585-9591.2004. PMID: 15331690 Free PMC article.

Abstract

Our previous studies with influenza A viruses indicated that the association of M1 with viral RNA and nucleoprotein (NP) is required for the efficient formation of helical ribonucleoprotein (RNP) and for the nuclear export of RNPs. RNA-binding domains of M1 map to the following two independent regions: a zinc finger motif at amino acid positions 148 to 162 and a series of basic amino acids (RKLKR) at amino acid positions 101 to 105. Altering the zinc finger motif of M1 reduces viral growth slightly. A substitution of Ser for Arg at either position 101 or position 105 of the RKLKR domain partially reduces the nuclear export of RNP and viral replication. To further understand the role of the zinc finger motif and the RKLKR domain in viral assembly and replication, we introduced multiple mutations by using reverse genetics to modify these regions of the M gene of influenza virus A/WSN/33. Of multiple mutants analyzed, a double mutant, R101S-R105S, of RKLKR resulted in a temperature-sensitive phenotype. The R101S-R105S double mutant had a greatly reduced ratio of M1 to NP in viral particles and a weaker binding of M1 to RNPs. These results suggest that mutations can be introduced into the RKLKR domain to control viral replication.

2

Restriction of viral replication by mutation of the influenza virus matrix protein.

Liu T, Ye Z. J Virol. 2002 Dec;76(24):13055-61. doi: 10.1128/jvi.76.24.13055-13061.2002. PMID: 12438632 Free PMC article.

Abstract The matrix protein (M1) of influenza virus plays an essential role in viral assembly and has a variety of functions, including association with influenza virus ribonucleoprotein (RNP). Our previous studies show that the association of M1 with viral RNA and nucleoprotein not only promotes formation of helical RNP but also is required for export of RNP from the nucleus during viral replication. The RNA-binding domains of M1 have been mapped to two independent regions: a zinc finger motif at amino acid positions 148 to 162 and a series of basic amino acids (RKLKR) at amino acid positions 101 to 105, which is also involved in RNP-binding activity. To further understand the role of the RNP-binding domain of M1 in viral assembly and replication, mutations in the coding sequences of RKLKR and the zinc finger motif of M1 were constructed using a PCR technique and introduced into wild-type influenza virus by reverse genetics. Altering the zinc finger motif of M1 only slightly affected viral growth. Substitution of Arg with Ser at position 101 or 105 of RKLKR did not have a major impact on nuclear export of RNP or viral replication. In contrast, deletion of RKLKR or substitution of Lys with Asn at position 102 or 104 of RKLKR resulted in a lethal mutation. These results indicate that the RKLKR domain of M1 protein plays an important role in viral replication.