Avian Influenza - Science topic

Can a Bird Flu Vaccine Protect Cows? A New Study Says Yes

Why This Matters

Bird flu (H5N1) is usually a problem for birds, but recently, it has been found in dairy cows. This raises concerns because cows produce milk consumed by humans, and the virus could potentially spread in unexpected ways. Scientists have now tested a bird flu vaccine on cows to see if it can protect them and if the immunity passes into their milk.

A new study published in Scientific Reports shows promising results: vaccinated cows developed strong immunity, and antibodies were even found in their milk. This could be a game-changer in preventing the spread of the virus. (Read the study here).

What Did the Study Find?

Researchers gave different doses of an inactivated bird flu vaccine to young cows (calves) and later to adult, milk-producing cows. They then measured the immune response in the animals’ blood and milk.

• Young Cows (Calves): The vaccine worked better with higher doses, producing stronger immunity.

• Milk-Producing Cows: Vaccinated cows not only developed antibodies but also passed them into their milk within two weeks.

This means that vaccinating dairy cows could help protect both the cows and potentially reduce the virus’s presence in milk.

What’s Next?

The study suggests that bird flu vaccines could be an important tool for protecting cattle and preventing further spread. However, more research is needed to:

• Test the vaccine in larger groups of cows.

• Monitor how long the immunity lasts.

• Improve the vaccine formula to make it as effective as possible.

Bottom Line

This study provides hope that a bird flu vaccine could help safeguard dairy cows and reduce risks to farmers and consumers. If successful on a larger scale, this approach could be a key step in managing bird flu outbreaks in cattle.

📖 Read the full study here: https://www.nature.com/articles/s41598-025-87831-w

Latest studies show emerging avian influenza virus in mammals especially cattles in USA. Does there is climate change involvement in this emergence?

This RG open question is linked to the previous about the dramatic evolution (partly unexplainable) of COVID19 in Northern Italy during wave 1.

The previous RG open question is reported below🔴 and resulted in a completely alternative model for the evolution🟨 of SARS-CoV/2 from pre-pandemic phase to pandemic phase.

In this specific RG question, the intention is to create an open discussion on the possible emergence of a violent outbreak of avian flu or similar in central Europe.

This concern arises from a qualitative model that links three events which in the past have always characterized the violent explosion of a bird flu or similar.

The model involves three steps.. https://www.researchgate.net/publication/367046404

This RG open question will serve to accumulate data both for and against this dire possibility.

Thanks to all the participants.

|--sv--|

🔴The novel Coronavirus in N. Italy, Lombardia 【 COVID19 / 2019nCoV / SARSCoV2 】 shows a fatality rate compatible with SARS-MERS. Why?? MAR.2020. -- https://www.researchgate.net/post/The-novel-Coronavirus-in-N-Italy-Lombardia-COVID19-2019nCoV-SARSCoV2-shows-a-fatality-rate-compatible-with-SARS-MERS-Why

🟨Link between the start of pandemic SARS-CoV/2 (COVID19) and the Huanan Seafood Wholesale Market in Wuhan (Hubei: China): the furin cleavage site of spike protein. FEB.2022. -- https://www.researchgate.net/publication/358443761

I study pathogenesis in different animal and i have mortality i need the equation

I am conducting Avian Influenza virus detection by real time rt PCR.

I did 4 target AI genes and 4 primer probe sets for PCR.

(H7 HA, H5 HA, NP and M target gene)

I run real time 4 time individually for that 4 target genes.

The result came out non-similarity.

(For Example,

In Sample no 1, H7 HA and H5 HA amplified (positive) but not amplified in NP gene and M gene .

In Sample no.2., result came all 4 gene were amplified.

In Sample no.3 NP gene and M gene and H5 HA gene came out positive result.)

How can I understand the nature of antigenic protein surfaces of virus and detection system of real time PCR.

Even though the same sample and same virus, can different results by using different target gene?

Im trying to find an oligoprimer set for HA gene amplification of H5N1?

I will appreciate if you could point out a primer set for phylohenetic analysis by H5N1 HA gene sequencing.

I am doing the hemagglutiantion elution assay for avian influenza, aiming to detect the balance between HA and NA activity. I mixed virus with 0.5% chicken erythrocytes on V-shaped hemagglutination reaction plates at 50 μl:50 μl and performed 2-fold multiplicative dilution, then incubated the plates at 4°C for 1h, then incubated the plates at 37°C for 6h and recorded the results every 1h. Theoretically, with the incubation condition at 37℃， NA activity can cut the agglutination linkage between red blood cells, at this time the positive wells of high dilution should turn negative first than the positive wells of low dilution, but it was found in the experiment that in addition to the phenomenon of turning negative in the positive wells of high dilution, the positive wells of low dilution also show a faster turning negative, even faster than the change rate of the positive wells of high dilution, I do not understand the reason behind this phenomenon. My positive criteria are no agglutination and no significant solid button in the wells, and the negative criteria are solid button and tear drop in the wells.

I have rescued two different avian influenza viruses: one using internal genes (PB2, PB1, PA, NP, M, NS) from H9N2 and outer genes (HA & NA) from H7N2 virus. The second virus was rescued using the same internal cassette from H9N2 and outer HA & NA from H7N8. After 293 T cells transfection by 24 h I changed the opti-Mem medium with Opti-Mem 0.3% which left on cells for additional 48 h. . Confluent MDCK cells in 6-well plate was inoculated with optim-Mem supernatant with addition of 1 ug/ml media trypsin TPCK. CPE started to appear 1-2 days post infection, followed by collecting supernatant from infected MDCK, tested and confirmed by RT-PCR against HA, NA and NP. PCR products for HA, NA & NP was confirmed positive too by sanger sequencing. However, when we passaged two viruses in 9-day old spf eggs NO HA titre came at all using 0.5% washed turkey RBCs Moreover, supernatant from infected MDCK did not show any HA titre as well despite it was positive by RT-PCR.

Greetings. I intend to detect Avian Influenza H5N1 in formalin fixed paraffin embedded chicken tissue section with H5N1 VN04-8 Monoclonal Antibody (3G2) (Catalog # 500-301-976, Thermofisher) by immunohistochemistry. So far, I did not find any article describing reactivity of this antibody for formalin fixed paraffin embedded chicken tissue section. My concern is, is this antibody reactive for formalin fixed paraffin embedded chicken tissue section? Kind thanks in advance.

Bird flu is a real threat. Lots species of aquatic birds migrate long distances. There are systems of rearing ducks in open water bodies in many countries. How do we really assess and predict scientifically the threat of avian influenza in such areas? Ecological studies? Immunological? molecular biological?Or Comprehensive long term studies?

In recent days, Iraq has lost many birds as a result of its elimination due to the outbreak of bird flu?

How the epidemic is transmitted to closed civilizations.

Do the bird migration season and its trends have an impact on the spread of the epidemic?

This pandemic is unique in many ways, but the fact remains that we can learn from past economic crises (for example, the global financial crisis) as well as from previous epidemics (for example, avian flu and swine flu, SARS, MERS, Ebola virus disease), which highlight the central role of employment, social protection and social dialogue in fight and recovery policies. In this regard, what lessons can be learned from this crisis?

How to calculate R_0, R_t, beta (the average number of contacts per person per time) and gamma? I try to defined SIR model, my data have infected, death and recovered. My country show the next information(I don’t know to calculate R_t) and I have the before said variable. Thank you.

I have done an experiment to study the persistence of avian influenza in lake water and in lake sediments. Do you know a good concentration method to use without the inactivation of the virus from water and sediments samples? I have to titrate the virus in MDCK cells.

Thank you very much,

Albert

Dear expertise,

Could someone can share with me a good protocol for flow cytometry based assay for titrating virus.

Hello everyone

I have 37% formaldehyde solution (formalin).I m working in avian influenza vaccine production.

Many articles mentioned 0.01% ,0.02% formalin inactivate virus .

But

How does I converted into 0.02% formalin from 37% formalin.

Then howmany ml of converted formalin should I add into allantoic fluid?

Virus to be isolated : Avian Influenza Virus

Analyzed samples : Tracheal swabs

specimens won't be processed for bacterial identification

I need information about Salmonella affecting exotic birds

It is clear that every year some new Avian Influenza sub types emerge in the sought east of Asia and then migratory birds carry them to other parts of the world

when i enter name of reference strains of h5n1 on genebank to get its fasta format not detected

Highly Pathogenic Avian Influenza (HPAI) commonly known as Bird Flu is a viral infection caused by strains of influenza that occur among birds. Veterinary extension and community interventions have a great effect in changing knowledge and practice toward avian influenza.

Iam working on pathotyping of avian influenza virus. I have sequenced some samples but it's quite difficult to detect HA cleavage site and presence of amino acids.

I have read that high levels of nucleocapsid protein of SARS can be found circulating in the blood. Is this true for other viruses e.g. avian influenza and Newcastle disease virus?

In another meaning, does bovine serum albumin have any role in attachment/entry phase of avian influenza virus during virus replication cycle? does this modulate virus uptake?

Hi, I will soon start working in the BSL3 lab with avian influenza viruses. Since they spread via aerosols, we are required to use facial protection, at least N95 or FFP3 mask. I used to wear a simple anti-dust FFP3 mask but after short-time use (about 1 hour) it was becoming unbearably uncomfortable, due to moisture build-up and feeling of not being able to breath freely. I will work in the BSL3 lab for at least 6 hours a day. Does anyone have any experience with the comfort of use of N95 masks for a prolonged time, or with any other kinds of facial protection that is more comfortable? PAPRs are out of our financial reach I'm afraid

Hi, I am trying to make avian influenza virus VLP. I have a recombinant plasmid expressing HA,NA and M1 genes. I am using Drosophilla melanogaster S2 cells for these protein expression. When I do Western blots of the cell lysates I see HA and M1 protein bands. However,I do not see any bands in the supernatant. Is it normal to detect these proteins only on the cell lysates before sucrose gradient purification? Also, in order to see if these expressed HA,NA nad M1 proteins have self assembled to form VLP do I take the cell lysates or cell supernatant for the sucrose gradient purification? Also, what volume of culture do I need to grow the cells to in order to get decent amount of VLPs?

Your help and advices will be very much appreciated.

As we know Avian Influenza virus is located at type A group of Influenza viruses. H9N2 sub type of Avian influenza make a lot of trouble for poultry Industry in Asia and Middle east. In some country the admantane drugs use for controlling impact of this disease. Unfortunately these viruses become resist to this group of drugs rapidly.

In the other hand, concern of reassortment and sharing drug resistance genes between this subtype and seasonal flu type A viruses are always a big issue in public health section.

in which HA bind to

My research proposal is about the antiviral effects of ginger against avian influenza virus. I was wondering if are there any other plants that could also be a potential antiviral agent for the said virus?

Want to know The diagnostic tests and screening tests for bird flu H5N1in India.

I expressed a hemaglutinin glycoprotein from Avian Influenza virus in an Adenovirus, I didnt see any HA, what would be the cause!? 

Next Generation Sequencing, Depth, Influenza Virus Genome

Western Blot can not detect the expression of protein, although the green fluorescence is expressed. Why ?

The vector is CMV promoter and the sequence is that eGFP-2A site-Myc-insert.

There are some MCS between 2A Site and Myc-tag.The cell line is 293T.The insert gene is a kind of polymerase which is from avian influenza.

I can perceive the green fluorescence frome the 293T cell by fluorescence inverse microscope.However,i can not detect the expression of my protein by Western Blot using Myc-antibody.Is the reason that the protein  which is a kind of virus's polymerase is a toxic protein for 293T cell and the protein is degraded? 

Hi All,

Is there any suggestions to reduce this backgrounds?

Thanks

For better understanding of pathogenesis of avain influenza virus. Also please provide the key for rapid diagnosis of avian influenza.

I need to inject day-old chicks with avian influenza virus for determination of intracerebral pathogenicity index (ICPI). Can any one guide me about the technique? What gauge of needle to use, what should be the depth and exact location for insertion of needle? I am unable to find details of the technique. Can any one help?

AIV allantoic fluid on WhatMan FTA cards.

http://www.bbc.co.uk/programmes/b05sxq9b#auto (go to 10mins 35 secs) - with a new variant of bird flu demonstrating a devastatingly mortality rate in the US, will culling halt the spread of H5N2?

There are H5N1 viruses which replicate to higher HA titer in SPF eggs. Does that mean those viruses are more adapted to poultry birds?

Any reference would be acknowledged.

Thanks

I usually use chick embryo (9-11 days old)  for inoculation of influenza in allantoic route. Has anyone used 13 days old chick embryo for allantoic inoculation of influenza and worked with him?

The question: Does anybody know scientific papers, measures or medicaments against the avian influenza H5N1 as reason for the death during March 2015 of more than 140 Dalmatian pelicans in Srebarna nature reserve (Bulgaria) and Danube Delta (Romania)?           Additional explanation: On 25 March 2015 21 Dalmatian pelicans from Srebarna nature reserve were found dead in the breeding colony. An avian influenza H5N1 was proved for two of them. Several days later over 100 Dalmatian pelicans from Danube Delta in Romania were found dead. Nobody knows what to do! It is not known if the arriving Great White Pelicans will be affected also. The problem is of great importance and urgency.

I want to design primers for H1N1 fragments. Are there universal primers for amplification of all the types of avian influenza?

We are seeing plenty of cases of vaccine failure as outbreaks of velogenic Newcastle disease and Infectious Bronchitis which are reported in in vaccinated flocks. How do you think should one investigate failures? If outbreaks occur in presence of sufficient antibody titres. Will virus isolation and sero-neutralization in ovo be enough. Or should one do challenge tests in vaccinated birds? 

Any suggestions?

Hello,

I'd like to start with reverse genetics of AIVs and it's the only thing that is not commercially available. Can anybody help me? Thanks.

Any suggested methods or literature that engage with the determination of viral load?

In  recent years several viral diseases like bird flu,avain flu, swine flu ,ebola etc has called panic in several countries. Such diseases nolonger remain localized but, lilely to be spread globally. What strategy should be adopted to combat these diseases. Since this being a global issue we should discuss how RG can help in this matter.

I tried 5 different gene combinations out of which I could rescue only 2 viruses. What could be the probable reason apart from the genetic stability of virions?

The macrophage and heterophil play key roles in this initial replication and dissemination  of AI viruses.

Can you tell me what is their role?

Another question:

What is the difference between mucinous degeneration and hyperplasia of goblet cell?

and what is the mechanism of them ?

What is the relationship between mucin gene and cytokine?

Does mucin contain cytokines?

This virus has genetic characteristics that concern, as already identified mutations in virus known to cause cases in mammals. Other mutations allow the virus is able to bind to cells in the upper airways that would make be transmitted from person to person. (see: Uyeki et al. Global Concerns (see: Uyeki et al. Global Concerns Regarding Novel Influenza A (H7N9) Virus Infections, New England Journal of Medicine, apr_2013).

Is it safe to perform experimental infection of poultry with low pathogenicity avian influenza viruses (LPAIVs) in the absence of biosecurity level-3 (BSL-3) facilities? Do they they pose significant risk for humans?

I want to design a vaccine using epitope prediction which is related to HLA, how the characteristics HLA can be using to design vaccine?

We have tried in PBS but the results looks quite weak.

Maybe you have different checked solution to propose?