Antiviral infection-fighting solutions -
See, a virus is a nanoparticle in which the weakest link is the fatty bilayer , and because soap dissolves fat, it causes the entire virus to fall apart and die.
So the soap actually physically breaks the viruses, deactivating it — no antibacterial compounds required! But remember, the ingredients should be alcohol, water, and maybe some essential oils or aloe vera, not a bunch of other chemical junk.
It is certainly not research, but the actress Kristen Bell posted an interesting image showing the difference under a UV light of microbes after hand washing vs. using hand sanitizer. So are there medications that are the virus equivalent of antibiotics? Yes, but antiviral drugs only work in very specific circumstances.
A key difference between antibiotics and antivirals is that antiviral drugs are effective only when administered within a certain time frame before or shortly after exposure.
And they do not destroy their target virus; instead, they inhibi t its development. Antiviral drugs become less effective with time and use, and have many side effects , like vomiting, cough, and behavioral changes. Okay, so now you might be wondering, what kills viruses without harming your gut microbiome and your immune system or causing serious side effects?
Natural antivirals. Viruses are tricky little organisms, and can come in all sorts of different shapes and forms, which makes treating them difficult. Luckily, there are some natural virus killers that you can incorporate into your life to help protect you against viruses.
Note that some of the items below are relatively new, and there are still questions about their effectiveness and risks. When it comes to what kills viruses naturally, antiviral herbs and supplements are the two most popular and easy to use options.
Clearly, you have a lot of different options when it comes to antiviral herbs! In terms of taking them, there are various methods. With some antiviral herbs, like oregano and basil, you can add them to your food as you usually would.
With other antiviral herbs, or if you want a more potent dose of basil or oregano, you can opt for supplements, teas, or liquid extracts. At the end of the day, what kills viruses is your immune system. Natural antivirals like silver, UV light, and antiviral herbs can definitely provide a helping hand, and sometimes a major one.
But ultimately, your overall health and the strength or your immune system will be what determines whether or not a virus you are exposed to makes you sick, and how long that sickness will last. To that end, the best thing you can do now to protect yourself against Covid — and against future viruses in general — is to take steps to keep your immune system strong.
However, we do have some concrete knowledge about what kills viruses naturally. Have you benefited from natural virus killers?
Which ones? Share your experience in the comments below! Trying to stay on top of wellness and health news and research can be overwhelming. We saved you the trouble. Here are After much research on line for how to treat a grape vine that was sickly, I found that it had a viral affliction.
One site said CINNAMON BARK. IT WORKED I used to suffer yearly with viral chest infections, and was very susceptible to flu. I decided to use an infusion of Cinnamon Bark and Liquorice root to top up my very weak black coffee, my regular drink, and have found that for more than 7yrs I have suffered no more than days of a mild cough in an average year.
Due to my age I regularly have the flu jab. Unlike previously, I have only mild tiredness as a reaction. Hopefully this may aid some people out there. Hi Ruth, thanks for letting us know, and that is incredible that you have only had a mild cough using cinnamon bark and licorice root!
Very interesting article. Thank you for the reminder of these wonderful things we can do to help ourselves.
Good information. Thank you. Surprised that garlic has not been mentioned. I regularly take garlic infused honey with clove and fennel as an immune system booster. Taking an antibiotic as directed, even after symptoms disappear, is key to curing an infection and preventing the development of resistant bacteria.
There are several different classes of drugs in the antiviral family, and each is used for specific kinds of viral infections. Unlike antibacterial drugs, which may cover a wide spectrum of pathogens, antiviral medications are used to treat a narrower range of organisms. Antiviral drugs are now available to treat a number of viruses, including influenza , human immunodeficiency virus HIV , herpes, and hepatitis B and C.
Like bacteria, viruses mutate over time and develop resistance to antiviral drugs. Modern medicine needs new kinds of antibiotics and antivirals to treat drug-resistant infections.
But the pipeline of new drugs is drying up. The last new class of antibiotics to be approved was the lipopeptides e. Major pharmaceutical companies have limited interest in dedicating resources to the antibiotics market because these short-course drugs are not as profitable as drugs that treat chronic conditions and lifestyle-related ailments such as high blood pressure or high cholesterol.
Antibiotic research and development is also expensive, risky, and time consuming. Return on that investment can be unpredictable, considering that resistance to antibiotics develops over time and eventually makes them less effective.
New antiviral drugs are also in short supply. These medicines have been much more difficult to develop than antibacterial drugs because antivirals can damage host cells where the viruses reside.
Today, there are more antiviral drugs for HIV than for any other viral disease, transforming an infection that was once considered a death sentence into a manageable chronic condition. But novel drugs are needed to combat other epidemic viral infections such as influenza and hepatitis B.
Several programs have been developed to stimulate research and development of new vaccines and medicines. Remember, as important as antibacterials are, they are useful only against infections caused by bacteria. For illnesses caused by other kinds of germs, antibacterials simply will not help your child get better.
They can actually add risks because of the possible side effects that all medicines have. At the same time, inappropriately used medicines can contribute to the growing problem of antibiotic resistance.
Every child gets a viral illness from time to time. Many viral infections affect the respiratory tract, which includes the nose, throat, and breathing passages where they can cause the common cold, the flu, a sore throat, and sinusitis. Viruses also can cause more serious illnesses such as acquired immunodeficiency syndrome AIDS , hepatitis, and rabies.
Because immunizations are available to protect your child against some viral infections eg, chickenpox, polio , make sure she is fully protected by all the vaccines recommended by the American Academy of Pediatrics.
Antiviral drugs are relatively recent developments, but an increasing number of these virus-fighting drugs are now available. They are made to prevent infection or shorten the duration of infections by preventing the virus from spreading, although they may not kill viruses that already exist.
Your pediatrician will be able to tell you when prescription antiviral drugs may be needed. Unlike broad-spectrum antibiotics, which are often useful against a wide range of bacterial organisms, antiviral medicines tend to be more specific and attack particular viruses.
Here are a few examples of antiviral drugs sometimes prescribed for children. Other medicines, called antiretroviral drugs, are used to combat infections caused by a particular type of virus called a retrovirus.
The most widely known retrovirus, human immunodeficiency virus HIV , is responsible for AIDS. Keep in mind that even though viral illnesses should not be treated with antibacterials, bacterial infections sometimes occur as a secondary complication of a viral disease.
In those cases, antibacterials can be used to treat the bacterial infection. Fungal infections are caused by microscopic plants whose spores become airborne and are breathed in by children. They can also enter the body through a cut in the skin.
When these spores are inhaled, they may settle in the lungs and begin to multiply and form clusters. Eventually they make their way into the bloodstream and travel throughout the body.
Like many infectious organisms, they can cause serious illnesses in children whose immune systems are already weakened by another disease such as cancer or AIDS. Some fungi can live in the body and never cause any sickness. Many drugs can fight these fungal infections. Some are over-the-counter medicines, while others must be prescribed by your doctor.
For serious fungal infections, pediatricians may select a medication called amphotericin B or newer antifungal drugs called azoles. Two of the most widely used azoles are fluconazole and itraconazole.
Some prescription antifungal drugs are not licensed for use in children, largely because little research has been done with youngsters.
Parasites can cause childhood infections. In some parts of the world, they are a common cause of illness and death.
Antiviral infection-fighting solutions in the world is newly infected with tuberculosis TB every second. In solutionw were an Ahtiviral 9. The vast Antiviral infection-fighting solutions of TB deaths are in the developing world, and more than half of all deaths occur in Asia. Search the National Academies Press website by selecting one of these related terms. The National Academies. Used properly, antibiotics can save lives.Antiviral infection-fighting solutions -
Several commercial cleaning products may kill harmful viruses. These products can contain various active ingredients and will usually advertise their effectiveness against viruses. Two active ingredients that household cleaning products commonly include are sodium hypochlorite and hydrogen peroxide.
These two chemicals are oxidizing agents and are capable of inactivating viruses. They do so by destroying the protein coating that protects the viral genetic material.
This means that the virus can no longer reproduce. Research suggests that both of these disinfectants are effective in inactivating coronaviruses on household surfaces. A study reported that alcohol-based hand rub solutions could inactive SARS-CoV-2, which causes COVID Several common herbs may also have antiviral properties.
Their concentrated plant compounds may act to kill viruses or reduce the symptoms of the resulting diseases. For example, oregano contains a key plant compound called carvacrol , which possesses antiviral properties that evidence suggests might be effective against SARS-CoV A study notes that compounds present in peppermint leaf extract exhibit antiviral activity against the respiratory syncytial virus.
Another study indicates that sage contains compounds that possess antiviral properties. Rosemary may also have antiviral effects. A study highlights that a compound present in rosemary called oleanolic acid displays an antiviral response against HIV and influenza.
Rosemary essential oil also shows antiviral activity against hepatitis A. Antiviral substances work to inhibit viral activity by preventing the virus from developing, replicating, and spreading. They fit under the antimicrobial umbrella but differ from antibacterial and antifungal products.
Antiviral substances include antiviral medications, which a doctor may prescribe to treat a viral infection. They also include masks and cleaning products, which may help prevent the spread of viruses, and some herbs, which have antiviral properties. Viruses such as the novel coronavirus are highly contagious, but institutions and individuals can take many steps to limit the spread of these viruses.
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Medical News Today. You can still access antivirals if you do not have a Medicare card but the cost for treatment will vary depending on your circumstances. Visit COVID oral treatments for people without a Medicare card for more information.
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Home COVID Testing and what to do if you have COVID Antivirals. COVID antivirals — your questions answered Answers to frequently asked questions about COVID antiviral medicines. On this page. COVID rapid antigen test updates From 1 October , you can no longer: register a positive rapid antigen test RAT result with Service NSW.
This is because the Service NSW RAT portal closed on this date collect free RATs at Service NSW locations. What are antivirals?
How do antivirals for COVID work? By reducing how severe the illness is, you are less likely to: go to hospital develop breathing difficulties need assistance with oxygen or intensive care treatment, or die from COVID What antivirals are available in NSW?
How do you take antivirals? Who is eligible to receive antivirals? You may be eligible to receive antiviral medicines if you are: 70 years of age or older 50 to 69 years of age with 1 additional risk factor for severe illness an Aboriginal person, 30 years of age or older and with 1 additional risk factor for severe illness 18 years of age or older and are immunocompromised.
What to do if you are at higher risk of severe illness. Talk to your doctor now so you know: which COVID test you should do if you get sick if you need antiviral medicines. Your doctor can fill out an action plan and you can discuss which treatment best suits you: Pre-assessment action plan for respiratory infections Pre-assessment action plan for respiratory infections in aged care facility resident If you test positive for COVID, your doctor will still need to provide a prescription for antiviral medicines but knowing which antiviral medicine is right for you will help you access it more quickly and easily.
How to access antivirals. Call your doctor straight away and tell them you have tested positive to COVID to discuss antivirals usually via telehealth.
Antivirals work best if taken as soon as possible, and within 5 days from when your symptoms start. If your doctor says you are eligible for antivirals, they will send you a prescription online or paper copy.
It's recommended you ask your pharmacy to arrange home delivery for your medication or ask someone to collect it on your behalf.
If symptoms become severe, call Triple Zero straight away and tell them you have COVID Why can't everyone access antivirals? Are there any side effects? Who are antiviral treatments not recommended for? How much do oral antivirals cost? More information. Fact sheet: Plan ahead if you are at higher risk of severe illness from COVID and flu - in your language.
Social tile: What COVID test should I do? Can I get antivirals? Please note: this resource is currently being updated. Amharic አማርኛ - What COVID test should I do? Arabic العربية - What COVID test should I do? Armenian հայերեն - What COVID test should I do? Assyrian ܣܘܪܝܬ - What COVID test should I do?
Vaccinia virus was used as the vaccine to eliminate smallpox — a devastating disease caused by variola virus that is currently an important bioterrorism concern 75 , Poxviruses have evolved various mechanisms to interfere with the activity of host cytokines, including IFN 77 , 78 , 79 , 80 Fig.
Uniquely, poxviruses encode soluble versions of cytokine receptors 'viroceptors' that intercept the normal activities of the target cytokines 81 , 82 , For example, the vaccinia-virus B8R protein binds soluble IFN-γ and prevents it from binding to cellular receptors This strategy to block the action of IFN-γ enables poxviruses to inhibit both the antiviral effects and, more importantly, the immune-regulatory functions of IFN-γ, simultaneously.
The IFN-γ receptor is highly conserved between members of the poxvirus family. Vaccinia virus that lacks the IFN-γ receptor is attenuated in vivo , although this deletion has no effect on virus replication in vitro 86 , Vaccinia virus and other poxviruses encode soluble interferon IFN receptors B8R and B18R that block the binding of IFNs to their cell-surface receptors.
The vaccinia virus E3L gene product is a double-stranded ds RNA-binding protein that inhibits activation of the protein kinase PKR and blocks IFN responses by sequestering dsRNA molecules.
The vaccinia virus K3L gene encodes a eukaryotic initiation factor 2, α-subunit eIF-2α homologue that interferes with PKR function by acting as a pseudosubstrate. The vaccinia virus VH1 phosphatase, a virion component, intercepts the IFN signalling pathway through dephosphorylation of signal transducer and activator of transcription 1 STAT1.
JAK, Janus kinase. Vaccinia virus uses at least two known functions to target PKR, which highlights the important role of this kinase in virus—host interactions. The vaccinia-virus proteins E3L 88 , 89 , 90 , 91 and K3L 91 , 92 , 93 , which are conserved in variola virus 94 , 95 , block IFN-mediated antiviral responses.
E3L encodes a dsRNA-binding protein that is involved in the inhibition of PKR 89 , 90 by interfering with the binding of PKR to dsRNA E3L might also prevent PKR activation by masking the substrate-binding domain K3L, a vaccinia-virus-encoded eIF-2α homologue 92 that potentiates translation by inhibiting PKR and eIF-2α phosphorylation 93 , 98 , acts by means of its homology to eIF-2α to interfere with the interaction of eIF-2α with PKR Deletion of the vaccinia-virus K3L gene reduced the ability of the virus to grow in IFN-treated cells 92 , and vaccinia virus devoid of the E3L gene was also sensitive to the antiviral effects of IFN As a dsRNA-binding protein, vaccinia virus E3L can also block other dsRNA-mediated antiviral pathways, such as the IFN-induced OAS enzyme 99 and IRF3 and IRF7 phosphorylation , which indicates that there are other mechanisms for the anti-IFN effects of E3L that are distinct from its inhibition of PKR.
Furthermore, E3L inhibits the adenosine-to-inosine editing activity of IFN-induced ADAR Although the amino-terminal domain of E3L is dispensable for infection of cells in culture, both the carboxy-terminal domain which is required for IFN resistance, binds to dsRNA and inhibits PKR and the amino-terminal domain of E3L were required for full pathogenesis in intranasal infections in a mouse model , which indicates the existence of dsRNA- and PKR-independent functions of E3L.
Interestingly, vaccinia-virus virion-contained phosphatase VH1 can bind to and dephosphorylate STAT1 , which indicates a new mechanism by which vaccinia virus interferes with the onset of host immune responses by blocking the IFN signalling cascade through the dephosphorylating activity of the viral phosphatase VH1 Ref.
The new technologies of functional genomics have had a marked impact on human biomedical research. In particular, global gene-expression analysis is now in widespread use in cancer and infectious-disease research, and it has become an integral part of the drug-discovery process , , Recent advances in proteomics have augmented this approach, making it possible to identify and quantify virtually all proteins that are present in a particular cell or tissue , and to characterize global protein—protein interaction networks in an organism Together, these technologies provide a global perspective on the complex interactions that occur between all levels of biological information 'systems biology' , from gene expression to protein production , Making sense of the huge amounts of data that are generated by these approaches requires highly sophisticated information technologies, which is the domain of the relatively new discipline of bioinformatics.
This confluence of genomic and information technologies brings a powerful new approach to the study of biological systems, as exemplified by recent studies The study of virus—host interactions and viral evasion of host defences will be revolutionized by these approaches.
Reports from the Cleveland Clinic on DNA microchip analysis of IFN-treated cells have already changed the field 14 , Before this high-throughput analysis was possible, it was thought that there might be, at most, 30, 40 or perhaps 50 IFN-regulated genes.
Now, their studies and our own G. This must change the way that a virologist thinks about viral strategies to evade host defences. The ever-increasing amount of microarray data that has been generated by examining virus—host systems has consistently shown that the expression of IFN and IFN-induced genes is differentially regulated in many systems and this phenomenon is not only limited to studies of virus—host interactions.
Studies with different members of the herpesvirus family best exemplify this point. IFN-induced genes are transcriptionally activated during human cytomegalovirus CMV infection.
Perhaps more interestingly, the addition of gB — the virion attachment protein — to cell cultures induces basically the same subset of genes that are induced by replication of the virus during a normal infection After infection with another herpesvirus, HSV, IFN-regulated genes were induced by a non-replicating mutant, but were inhibited by the wild-type virus, which indicates that virus replication is necessary to suppress the host-defence IFN response in this HSV system In related studies, we have found by microarray analysis that heat- or UV-inactivated influenza virus, which attaches to host cells, but does not replicate, also induces the expression of a substantial subset of the same genes that are dysregulated during a productive infection Interestingly, the cellular IFN response to influenza-virus infection is viral-strain specific.
The PR8 strain induces the synthesis of several IFN-induced genes, whereas the WSN strain dysregulates very few IFN-induced genes. We speculate that this might account for the neurovirulence of WSN a reduced IFN response allows increased viral replication , which might be due, in part, to the NS1 gene product.
Little is known about how certain viruses trigger the IFN response or how this might occur as a result of viral attachment. It is widely thought that viral dsRNA intermediates that accumulate during the course of replication are the primary mediators that trigger IFN production.
However, dsRNA is not present when inactivated virus or a viral attachment protein is used unless contamination is a factor.
We have carried out microarray analysis of dsRNA-treated cells that lack all type I IFN genes So, the possibility of gene induction by autocrine actions of IFN was eliminated.
More than genes were stimulated and nearly genes were repressed — all in the absence of an IFN response. Different inflammatory cytokines and viruses also induced a subset of these dysregulated genes, which shows that there are interconnections between disparate pathways.
Induction and repression of such a diverse family of genes has profound implications for virus—host interactions: this is a lot for the virus to cope with. Another advantage of these high-throughput approaches is best illustrated by our work on HCV and microarrays.
Many groups, including our own, have shown that the HCV NS5A protein confers type I IFN resistance, at least in part, through the inactivation of PKR , , , , To get a wider view, we carried out microarray analysis on cells that had been treated with type I IFN in the presence or absence of NS5A or a mutant NS5A that is unable to bind PKR G.
Our goal was to define the molecular mechanisms that make HCV resistant to IFN treatment. At the same time, we were able to carry out a high-throughput analysis of the global effects of treating cells with IFN.
Remarkably, we observed that a distinct subset of IFN-regulated genes were downregulated after treatment with NS5A, some of which were not downregulated by the NS5A mutant that is unable to bind PKR.
Another microarray approach was used to examine transcriptional profiles in chimpanzees infected with HCV Prominent among these were many IFN-regulated genes, including STATs, IRFs, Mx proteins and OAS. Remarkably, the level of expression of some of these genes was altered nearly fold.
Therefore, it is not surprising that HCV must encode anti-IFN strategies. The greatest challenges for the future will involve designing and developing better antiviral therapeutics, perhaps in conjunction with an IFN that has been made more potent by molecular-breeding technologies Box 4.
But, we desperately need a strategic plan. One possibility is to determine whether all viruses or all RNA viruses, or all DNA viruses, or all respiratory viruses and so on use common strategies to survive in the host and successfully replicate.
We propose the establishment of a 'virus compendium' or a database that summarizes the events that occur during infection by all mammalian viruses Fig. This database should comprise both microarray transcriptional-profiling data and high-throughput proteomics information.
Data should be assembled from various experimental systems, including in vitro infection systems, animal and human models, and surrogate systems such as the HCV replicon system. Using sophisticated software, such as Resolver TM and the proteomics software that has been developed at the Institute for Systems Biology, it should be possible to define common cellular pathways that are affected by virus infection or by overexpression of a viral protein.
Such an approach might lead us to the development of broadband antivirals — 'virus silver bullets' — which would be effective against a wide variety of viruses, just as antibiotics are effective against many different species of bacteria.
The virus compendium will use high-throughput, genomic-scale techniques to analyse various virus—host interaction systems, many of which could be improved or developed by molecular-evolution approaches, such as DNA shuffling Box 4.
The collection of data sets will be integrated in compendium databases and will be subject to data mining, with the aid of bioinformatics and computational analysis. It is to be hoped that, as indicated by pilot studies, this effort will help us to understand consensus and pivotal pathways, targets and strategies during various virus—host interactions.
This collection of data and knowledge will not only facilitate our search for new antiviral compounds and vaccines, but will also be useful in related areas, such as microbial pathogenesis, immunity and cell biology. This effort deserves the attention of the scientific community and requires proper cooperation and coordination of the research programmes at many institutions, both public and private, academic and industrial.
An emerging theme in the interferon IFN field is the cross-talk that occurs between the main cellular regulatory pathways. TLRs are a family of innate immune-recognition receptors that recognize molecular patterns that are associated with microbial pathogens, and they induce anti-microbial immune responses The link between TLRs, IFNs and viruses became evident from the report that TLR3 recognizes double-stranded ds RNA which is often a by-product of virus replication This interaction results in the activation of nuclear factor-κB NF-κB and the production of type I IFNs.
Double-stranded RNA also induces the expression of IFNs by TLR-independent mechanisms and activates several of the IFN-induced proteins and enzymes. It is not yet clear whether TLR3 is a bona fide receptor that induces IFN production in response to viruses, but it is intriguing that mice that have deletions in the protein kinase PKR , RNase L and myxovirus-resistance Mx genes can still respond to dsRNA or viral infection.
This indicates that there are further pathways possibly through TLRs for viral recognition by host cells It will be interesting to monitor the infection of TLR3-deficient mice with various viral pathogens. A recent report concerning TLR4 is also of note. Horng et al. have identified and characterized TIRAP, which controls the activation of MYDindependent signalling pathways downstream of TLR4 Ref.
Importantly, these investigators found that PKR is a component of both the TIRAP- and MYDdependent signalling pathways. Even more remarkably, P58 IPK — the influenza-virus-activated cellular inhibitor of PKR — was also found in a complex with TIRAP and PKR, which indicates that PKR and its regulators including the PKR activator PACT might be downstream targets that are activated by TIRAP.
The primary players in the interferon IFN signalling pathways are the signal transducers and activators of transcription STATs and Janus kinases JAKs , see figure.
STATs are latent transcription factors that become tyrosine phosphorylated by the JAKs. The JAKs phosphorylate and activate the STATs, which homo- or heterodimerize and translocate to the nucleus to induce the expression of the IFN-stimulated genes ISGs.
The STAT1—STAT2 heterodimer complexes with nuclear protein p48, and this complex binds to the IFN-stimulated response element ISRE sequences in the promoters of ISGs.
STAT1 and STAT3 homo- and heterodimers bind to γ-IFN-activated sequence GAS elements. In addition, the mitogen-activated protein kinase MAPK pathways involving extracellular-signal-regulated kinase ERK and p38 MAPK have a role in IFN signalling, by phosphorylating serine residues of STAT1 and STAT3 and further enhancing their transcriptional activity.
Type II IFN signalling follows a similar, but distinct, pattern. This regulation is distinct from that of the IFN-γ pathway, which relies on STAT1 homodimers for activation through the GAS element. Most of the components of these complex signalling pathways have been targeted for disruption in experiments using knockout mice , These mouse experiments have validated the importance of these host pathways in fighting virus infection.
Of the influenza viruses, type A viruses cause the most illness and have caused three important worldwide outbreaks during the past century The influenza pandemic of was remarkable for many reasons. Twenty-eight per cent of the world's population million people were potentially infected during the pandemic.
Estimates of the total mortality that resulted from this pandemic range from 20 million to 40 million people It was proposed — in retrospect, in a somewhat naive way — that the ability of viral non-structural protein NS1 to combat the interferon IFN response was the main determinant of virus pathogenicity in — Although it is still too early to completely discount this theory, it seems that the pandemic-type NS1 in a WSN-influenza-virus background actually attenuates virulence in vivo However, the studies were carried out in mice and the WSN virus that was used in these studies was mouse adapted.
In this study, WSN virus induced the expression of some IFN-stimulated genes ISGs to high levels. By contrast, infection with recombinant WSN virus carrying the pandemic flu NS1 gene failed to significantly induce the expression of any ISGs, and the levels of the myxovirus-resistance protein MxA and ISG15 were markedly reduced.
Studies using a better animal model preferably a non-human primate such as the Asian macaque are required to fully understand the role of NS1 in pandemic influenza. Therefore, the hunt continues for the cause of this great pandemic, looking at both viral and host factors that might have affected virus replication and virulence DNA shuffling, pioneered by Maxygen, Inc.
It is a method for quickly evolving genes, operons and whole viruses for the acquisition of any desired properties. This has been accomplished for the generation of new retroviruses that have altered tropisms , but more relevant to this review, also for the generation of new cytokines.
DNA shuffling of a family of more than 20 interferon-α IFN-α genes was used to derive mutants or variants that have increased antiviral and antiproliferative activities in mouse cells Normally, the effects of IFN are species specific, such that human IFN works on human cells and mouse IFN works on mouse cells.
There is minimal cross-species reactivity of these IFNs, except perhaps at very high concentrations. In the shuffling experiment, the most active human IFN clone was improved ,fold relative to human IFN-α2 a in mouse cells.
Impressively, the three most active human clones were more active than native mouse IFN-α. Sequence analysis of the chimaeras showed that the sequence of the carboxy-terminal residues — correlates with the unusually high activity in mouse cells, which is consistent with previous site-directed mutagenesis studies On the basis of functional experiments and modelling, the residues in this region are proposed to interact with the mouse IFN-α receptor.
The implications of this approach are profound. It will be of great interest to determine why the shuffled IFNs are so much more potent. Is it only due to enhanced receptor interactions?
It will be interesting to carry out DNA-microarray analysis of cells that have been treated with these highly evolved cytokines. It will also be important to test whether these IFNs are active against hepatitis C virus in a replicon assay based on human liver Huh-7 cells, as these IFNs have only been tested so far against mouse encephalomyocarditis virus EMCV , which is a particularly IFN-sensitive virus.
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This study examined the effects of NS1 protein expression during influenza A virus infection on global cellular mRNA levels using high-density microarrays. It indicated that the cellular IFN response to influenza A virus infection in lung epithelial cells is influenced markedly by the sequence of the NS1 gene, and it characterized a virus that contains the pandemic influenza NS1 gene.
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