Mechanisms of Viral Defence, Infection and Recovery

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A Virus is an ultramicroscopic infectious agent.

The H1N1 A 2009 (Swine Flu)  is a novel strain of the influenza virus.

Viruses cannot reproduce on  their own. To reproduce, a virus must bind to a living cell inside some organism, insert its genetic material into that “host” cell, and take over the cell’s reproductive “machinery.” The virus then makes copies of itself – maybe hundreds of thousands. Sooner or later, this kills the infected cell – causing the virus to leave the cell and cause illness. Once out of the host cell new viruses start the process over, attacking other cells until the immune system, and or medication controls their activity and replication. The H1N1 Influenza A virus once inside a cell can produce approximately 100,000 new virions in about 8 hours.


A person with H1N1 (swine flu) appears to be able to spread it to others for one (and possibly two) days before symptoms first occur. This is because a person infected with swine flu virus may have it present in their nose, mouth and throat for one to two days before they get symptoms. Spread of infection can continue for up to 7 days after symptoms first appear. Children, especially younger children, might potentially be contagious for up to 10 days.The virus replicates in the cells lining the nose and are coughed or sneezed out in droplets of mucous. A single sneeze can contain 40,000 droplets, a single one may be all that is required to cause infection.

Viruses Must First Circumvent The Mucosal Immune System.

Mucosal immunity is important for long-term protection and forms a first line of defence against mucosally transmitted pathogens such as influenza. Mucosal defence against pathogens consists of both innate barriers, such as mucous, epithelium, and innate immune mechanisms, and adaptive host immunity. The latter consists predominately, at mucosal surfaces of specialised thymic derived cells called CD4+ T cells, secretory immunoglobulin A (SIgA), secretory immunoglobulin M (SIgM) and antigen-specific (memory primed) cytotoxic T-lymphocytes (CTLs). Although not confirmed SIgM may compensate for IgA deficiency in the gut and lungs.

If the infective assault on mucosal tissues is successful, by intracellular pathogens such as a virus it will result in the induction of cell-mediated immunity. This includes the production of CD4+ T helper-type 1 cells, as well as CD8+ cytotoxic T-lymphocytes. These responses are normally accompanied by the synthesis of secretory immunoglobulin A (SIgA) antibodies, which provide an important first line of defence against invasion into deeper tissues by these pathogens. It is possible to stimulate the B cells and plasma cells to increase production of SIgA and SIgM by using colostrum and Saccharomyces Boulrdii two natural agents of immune support.

The H1N1 Swine Flu virus is a novel strain of influenza. Existing vaccines against seasonal flu provide no protection, and there is currently no vaccine for this strain. A study at the U.S. Centres for Disease Control and Prevention published in May 2009 found that children had no preexisting immunity to the new strain but that adults, particularly those over 60, had some degree of immunity

Experts writing in the July New England Journal of Medicine note that “historically, pandemic viruses have evolved between seasons, and the current strain may become more severe or transmissible in the coming months.” The H1N1 swine flu variant may be prone to reassortment ( Reassortment is the mixing of the genetic material of two similar viruses that are infecting the same cell) and mutation. NEJM Influenza Centre contains further information of value.

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20 Comments. Leave new

  • Just to say thank you for the quality of this useful info.

  • Sally Gordon
    July 29, 2009 10:16 am

    Thank you for providing such useful, easy to digest material and a workable protocol.

  • Anne Pemberton
    July 29, 2009 11:06 am

    This is great! Comprehensive coverage without overload, which is really improving my understanding.

  • Harriet Jedwab
    July 29, 2009 11:45 am

    Very helpful – thank you

  • Jeanette stamp
    July 29, 2009 12:52 pm

    Thank you so much for all this excellent information – very helpful and reassuring.

  • Frances Ross
    July 29, 2009 12:53 pm

    Thank you for the info. Quick question. How long is it safe for someone to take saccharomyces boulardii – especially if this pandemic is thought to mutate and get stronger in the autumn and winter.

    • Michael Ash
      July 29, 2009 6:27 pm

      Dear Frances.
      The long term consumption of Saccharomyces Boulardii has no contraindications unless your intended consumer is yeast allergic – that is they have an IgE responce to yeast not an IgG response in which case they should never have it at all.
      There is a question about whether the antigenic effect of the SB in terms of promoting SIgA declines over time. This has been addressed by finding a different manufacturers strain and rotating the two products to avoid developing immune tolerance to the product. In clinical experience this has varied, based on regular testing from changing every 2 months to not at all.

  • Natalie Gillan
    July 29, 2009 1:11 pm

    Most helpful. The protocols are workable and easily applicable

  • Great article, really useful. I being asked for nutrition based protection from swine flu all the time so will definitely be using a lot of the material covered here. Many thanks and please keep up the posting of these valuable papers



  • Lisanne Davidson Dip ION
    July 30, 2009 3:03 pm

    Thank you Michael and Antony for all the excellent information you continue to provide on this situation. Already clients have been reassured, and are very happy to follow the guidelines as presented; it helps people make informed choices which is excellent!

  • Hello again, one quick question, you mention in the paper that people are at risk of spreading the virus once they are symptomatic, but isn’t it true that they can still spread the virus before becoming symptomatic?

    I have a lot of clients coming to see me about this at present; plus I am being asked to run workshops and write articles on how to boost the immune, so your protocols & research papers are proving extremely useful, many thanks once again.

    • Dear Angela
      A person with H1N1 A 2009 (swine flu) appears to be able to spread it to others for one (and possibly two) day before symptoms first occur.
      This is because a person infected with swine flu virus may have it present in their nose, mouth and throat for one to two days before they get symptoms. Spread of infection can continue for up to 7 days after symptoms first appear. Children, especially younger children, might potentially be contagious for up to 10 days.The virus replicates in the cells lining the nose and are coughed or sneezed out in droplets of mucous. A single sneeze can contain 40,000 droplets, a single one may be all that is required to cause infection in someone with a less than optimal mucosal defence.

      Primary transmission – infected person exhales infected droplets –healthy person inhales them directly

      The key point is that infection risk involves transmission – if the infected individual does not sneeze, laugh or cough, or wipe mucous onto a surface – and you or anyone else has no contact, the virus will not be transferred – no risk of infection will occur.

      Secondary transmission: infected person touches droplets, or droplets fall onto hands or surfaces –healthy person touches infected hand or surfaces including countertops, door knobs, towels, money, books and clothing etc. and then rubs nose, mouth or eyes.

      Airborne Transmission occurs when viruses travel on dust particles or on small respiratory droplets, or they may become aerolised when people exhale and act like invisible smoke. They can then travel some distance on airborne currents, meaning it may not be necessary to be in direct contact with someone to become ill.

      Influenza Virus Survival: Depends on humidity and warmth, it is able to survive for 24-48 hours on plastic and stainless steel. On cloth paper and tissue 8-12 hours but transferable to hands for about 15 minutes. It will only exceed survival on the hands by five minutes if the viral load is high.

  • There is some talk that if WHO orders it, member nations must begin forced vaccination. Whenever I get a flu shot, I seem to get sick. (I use them to pick the time of my illness, not whether or not I get it.) Will the nutritional preventives discussed here protect against the effects of the vaccination as well as the disease? And would that be a good thing? If the immune system is fortified enough, won’t it just shrug off the illness without “learning” the specific antibody defenses the vaccine was intended to stimulate?

    • Dear Rick
      Thank you for your question. There is a powerful immunological ideology in the vaccination proponents, that the antibodies and T cells that are primed for the purpose of early recognition and elimination of pathogens, including the influenza virus is the most effective means of reducing mortality and morbidity.

      There is of course a ‘dirty little secret’ in immunology, that is the adaptive (memory) immune system cannot respond to the weakened pathogen in the vaccine without the presence of a suitable adjuvant to agitate the innate system first. This is of course one of the current controversises about vaccination – does the adjuvant cause secondary long term health problems to the immunologically vulnerable?.

      The comprehension that the innate immune system is so important has turned immunology upside down over the last decade or so as labs, university’s and private companies have begun picking apart the mechanisms in innate immune defence. Once seen as the poor cousin, innate immunity is quite the belle of the immunological ball.
      Is vaccination recommended? A recent (2005) meta-analysis in the The esteemed Lancet Journal, concluded,

      “In elderly individuals living in the community, (influenza) vaccines were not significantly effective against influenza, influenza-like illness, or pneumonia.” The conclusion stated: the overall effect of flu shots is “modest,” at best.[1]

      “Modest” is a complicated medical term that means “not much.”

      In 1992, the British epidemiologist, Edgar Hope-Simpson, wrote that understanding influenza’s..

      “..seasonal factors (summer vs winter) may be of critical value in designing prophylaxis against the disease.”

      In effect, he was reminding us that the key to influenza prevention may not be down the road of ‘boosting’ acquired immunity by influenza vaccination but rather through better understanding and use of innate immunity. The Transmission of Epidemic Influenza (The Language of Science) By Edgar Hope-Simpson

      Unlike the constantly evolving ‘adaptive’ immunity, ‘innate’ immunity is a remarkably sophisticated branch of host defense that is “hard-wired” to respond rapidly to microorganisms using genetically encoded effectors that are ready for activation by an antigen before the body has ever encountered that antigen.

      This means if you follow the optimal mucosal health programme you are looking to reduce viral load, viral penetration and viral replication. If the barriers are breached it is also hoped – but not proven, that the increased Vit D status will moderate immune responses to the H1N1 virus, reducing risk of adverse cytokine production, but optimising viral elimination.

      Mass vaccination? – There remains good indication that combining vaccination with optimal mucosal health and hygiene will provide an effective triple strategy. Is there a viable reason for mass vaccination? – I think the jury is out on this. My view, is that if transmission is contained (such as through the use of effective masks, and hygiene practice) and innate immunity is optimal the need for vaccination declines in value. If the former is impossible or avoided then vaccination value increases.

      Failure to obtain memory status? – This is a good question; will the avoidance of exposure mean no future resistance embedded in the immune memory. There in lies the difficult decision, no exposure – no immune memory, little exposure – possible immune memory, significant exposure, immune memory and or illness and risk. As the Influenza virus mutates so quickly, long term immune memory has little benefit if the genetic changes mean the immune memory cells are fooled. Best outcome – avoid illness, or limit effects of illness – your choice.

      The influenza virus has two important aspects to consider in terms of immune memory. The antigenic drift where changes in proteins by genetic point mutation and selection occur reflects the requirement for an annualised vaccination programme – if vaccine defence is your choice. Antigenic shift occurs (only in Influenza A because of multiple organisms being infected) when two viruses enter a cell at the same time and create through changes in proteins via genetic re-assortment an entirely different virus not covered by annual vaccine or prior exposure.

      The influenza virus is very vulnerable to genetic changes because of the speed of gene replication once in the infected cell and the numbers of replication errors that occur. Pre-existing immunity (natural or provoked) also applies a developmental pressure to mutate to the virus as it looks to avoid destruction. Immunisation in effect determines mutation and viral strain development.

      Reducing adverse effects of vaccination? – This is less clear, there are indications that a valid Vit D status i.e 25(OH)D above 50 ng/mL, assures you are not suffering from substrate starvation, that is, your body has enough Vitamin D for its needs and some left over to store. At a level of 30 ng/mL, most people are still suffering from Vitamin D substrate starvation.[2] As Vit D is increasingly understood to manage over enthusiastic immune responses, this would seem a sensible, low risk intervention.

      [1] Jefferson T, Rivetti D, Rivetti A, Rudin M, Di Pietrantonj C, Demicheli V. Efficacy and effectiveness of influenza vaccines in elderly people: a systematic review. Lancet. 2005 Oct 1;366(9492):1165-74. Epub 2005 Sep 22. View Abstract
      [2] Heaney RP, Armas LA, Shary JR, Bell NH, Binkley N, Hollis BW.25-Hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions.Am J Clin Nutr. 2008 Jun;87(6):1738-42. View Abstract

  • Sir,
    What is about subclinical attack of swineflu.?

    Is there any use of TULASI in immunity in general & for swineflu.?

    Person living in area of swine for long period / in childhood /visited does have good amount of immunity even if muted virus are there ?

    • Dear Ajit – Thank you for your questions.

      Subclinical swine flu – I am not sure what you mean, but if it implies that the individuals natural defence suppresses viral expansion to the point of significant reduction of symptoms then this will imply either that there is an effective innate defence system limiting viral cell penetration or that the virus is one the person has some adaptive immunity to, and is therefore not the H1N1 2009 (Swine Flu), unless that person is over 60 (some people of this age do have an element of adaptive immunity), as there is no available evidence to confirm that there is any prior exposure to this unique genetic combination – hence no adaptive memory cells.

      Tulasi or Holy Basil has some evidence of immune effect. Holy basil is thought to have antiemetic, anticancer, hypoglycemic, hypotensive, sedative, antimicrobial, antiviral, anti-inflammatory, antipyretic, analgesic, and antiulcer activity.
      1. Singh S, Majumdar DK. Effect of Ocimum sanctum fixed oil on vascular permeability and leucocytes migration. Indian J Exp Biol 1999 37:1136-8
      2. Agrawal P, Rai V, Singh RB. Randomized placebo-controlled, single blind trial of holy basil leaves in patients with noninsulin-dependent diabetes mellitus. Int J Clin Pharmacol Ther 1996;34:406-9.
      3. Godhwani S, Godhwani JL, Vyas DS. Ocimum sanctum: an experimental study evaluating its anti-inflammatory, analgesic and antipyretic activity in animals. J Ethnopharmacol 1987;21:153-63.
      4. Kar A, Choudhary BK, Bandyopadhyay NG. Comparative evaluation of hypoglycaemic activity of some Indian medicinal plants in alloxan diabetic rats. J Ethnopharmacol 2003;84:105-8.

      As you can see these are a mix of animal and human studies. The use as a prophylactic is less clear. It may be possible to use in the management of fever. There is no substantive evidence that it will have an effect in the prevention of a novel virus, and no published data on the management of the innate immune system. In my view it has a less compelling support base than the nutrients discussed. However, I am not a herbalist and may well have missed some other studies that do provide additional support.

      Exposure to swine does not impart any adaptive immunity to the new H1N1 virus. This virus is a combination of genes (8) that have coalesced into a previously unseen combination. As the adaptive immune system will have had no exposure to this combination there will be no inherited memory. However, a healthy barrier and antiviral peptides do appear to confer some level of resistance.

  • A swine flu patient is serious and on respirator , that is having symptoms for last 15 days from first appearence of symptom, has been started with tamiflu 75 mg bid for 5 dayson 8 th day after first symptom appear

    so is this patient is infective on 15 th day of his illness ?

    in short for how many days after he can be infective after disappearence of all symptoms when he is with symptoms with respiratory complications ?


    • Dear Ajit
      Please understand I am unable to make individual recommendations but can make general observations. Assuming your patient was infected by the H1N1 novel virus it is unlikely due to the time period and the medication that they are still infective or indeed infected by the novel virus. It sound more likely that he has had secondary complications.
      Among persons experiencing secondary events or complication infected with previous variants of swine influenza viruses, clinical syndromes have ranged from mild respiratory illness, to lower respiratory tract illness, dehydration, or pneumonia. Deaths caused by previous variants of swine influenza viruses have occasionally occurred.

      Although data on the spectrum of illness is not yet available for this novel influenza A (H1N1), clinicians should expect complications to be similar to seasonal influenza: exacerbation of underlying chronic medical conditions, upper respiratory tract disease (sinusitis, otitis media, croup) lower respiratory tract disease (pneumonia, bronchiolitis, status asthmaticus), cardiac (myocarditis, pericarditis), musculoskeletal (myositis, rhabdomyolysis), neurologic (acute and post-infectious encephalopathy, encephalitis, febrile seizures, status epilepticus), toxic shock syndrome, and secondary bacterial pneumonia with or without sepsis.

      There is no colated data available to clarify periods in which the patient remains infective after onset, but one should consider 10 days excluding intervention and to be sure, until you have a nasal swab confirmation up to 15.


  • Sir,

    i have questioned a imaginery case and not a actual case,
    my question is ” FOR HOW MANY DAYS A COWER RESPIRATORY COMPLICATED CASE REMAIN INFECTIVE AFTER GIVING A FIVE DAYS TAMIFLU TREATMENT AND STILL REMAIN SERIOUS ” so as to take care for attending doctor , nursing staff , relatives ,……..


    • Dear Ajit
      There is no collated data available to clarify periods in which the patient remains infective after onset and post treatment with Tamiflu, but one should consider 10 days from confirmation of infective symptoms ‘excluding intervention’ and to be sure, until you have a nasal swab or other approved lab test confirmation of resolution up to 15.

      So if your example patient presented days after symptoms developed, and had 5 days of Tamiflu, without apparent resolution of respiratory symptoms, a conservative estimate is to allow an additioal 8 days in which transfer of H1N1 novel virions may be possible.
      There are also early indications of resistance to available treatments:

      Our results indicate that the same neuraminidase mutation (H275Y) is associated with oseltamivir resistance not only in seasonal H1N13 and avian H5N14 viruses but now also in 2009 pandemic H1N1 strains. We hypothesise that the presence of subtherapeutic levels of oseltamivir at a time when viral replication had already begun was an important factor that led to the emergence of the resistant virus in the father of our index patient. Other oseltamivir-resistant strains of 2009 H1N1 virus detected during postexposure prophylaxis have been reported to the World Health Organization

      [1]Antiviral use and the risk of drug resistance: pandemic (H1N1) 2009 briefing note 12. Geneva: World Health Organization, September 25, 2009. (Accessed November 9, 2009, at

      This does imply that in some cases the patient will remain infectious post treatment as the tetment is resisted.



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