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Update on S-OIV or A (H1N1) Influenza (formerly Swine Influenza) - May 1, 2009

Until further notice, I am going to devote my blog to updates on the A (H1N1) influenza situation. I will post again about outdoor medicine once the flu situation settles.

The following post is derived from information provided by the Santa Clara County (California) Health Department:

We are now referring to "swine influenza" or "swine flu" as influenza A (H1N1) or S-OIV (swine-origin influenza virus).

As of May 1, 2009, the United States has confirmed 141 cases of S-OIV. In contrast to the cases reported from Mexico that have been more severe, the majority of U.S. cases have thus far been characterized as mild. Because of evidence of sustained human-to-human transmission, the World Health Organization raised the pandemic alert level to Phase 5. The outbreak strain of swine-origin influenza A (H1N1) virus (S-OIV) is susceptible to oseltamivir (Tamiflu) and zanamivir (Relenza), but resistant to amandatine and rimantadine.

Because of the high number of patients who are concerned about whether or not they are suffering from S-OIV and the mild profile of the vast majority of U.S. cases, it is becoming necessary in certain locations to prioritize testing for patients in high risk settings for whom a positive result would necessitate a public health action or decision (such as school closure) or for patients who are seriously ill, in order to help doctors, public health officials, and epidemiologists understand disease patterns and severity.

It is currently being recommended to test patients for S-OIV if they are:

• Hospitalized persons with influenza-like illness (fever greater than 37.8°C [100°F] AND at least two of the following: runny nose or nasal congestion, sore throat, or cough; OR if they suffer from pneumonia. Some instructions use a slightly higher temperature (38°C [100.4°F]) as an indicator.
• Non-hospitalized persons with influenza-like illness if they are in a congregate setting: such as school, daycare, or university; jail; homeless shelter; or long-term-care facility.

The usual test is a nasal swab to test for influenza virus. This is not a test specifically for S-OIV, but only for influenza A or B. False negative tests for influenza A are possible. If the test if positive for influenza A, the sample must be further tested ("typed") to determine the presence or absence of S-OIV. A rapid influenza test that is positive for influenza B is of some reassurance, because concurrent S-OIV (a form of influenza A) infection is unlikely.

When a person is suspected or known to have S-OIV infection, and the case is mild (e.g., does not require hospitalization), then the patient is instructed to self-isolate at home, and asked not to attend work or school for 10 days after the start of illness, or until all symptoms have resolved (whichever is longer).

Guidance for care at home of persons with A (H1N1) influenza can be found at
http://www.cdc.gov/swineflu/guidance_homecare.htm

The Centers for Disease Control (CDC) considers the definition of a confirmed case of S-OIV infection to be a person with an influenza-like illness with laboratory confirmed S-OIV infection at the CDC by reverse transcriptase polymerase chain reaction (RT-PCR) or viral culture. A probable case of S-OIV infection is defined as a person with an influenza-like illness who is positive for influenza A, but negative for H1 and H3 by influenza RT-PCR. A suspected case of S-OIV infection is defined as a person with influenza-like illness:

• with onset within 7 days of close contact with a person who is a confirmed case of S-OIV infection, or
• with onset within 7 days of travel to a community either within the United States or internationally where there are one or more confirmed cases of S-OIV, or
• who resides in a community where there are one or more confirmed S-OIV cases.

The estimated incubation period for S-OIV infection is unknown and could range from 1 to 7 days, and more likely from 1 to 4 days. Persons with S-OIV infection are assumed to be shedding virus (and to be contagious) from the day prior to illness onset until resolution of symptoms. Persons with S-OIV infection should be considered potentially contagious for up to 10 days following illness onset. Persons who continue to be ill longer than 10 days after illness onset should be considered potentially contagious until symptoms have resolved. Children, especially younger children, might be contagious for longer periods.

When indicated, antiviral treatment should be initiated as soon as possible after the onset of symptoms. Evidence for benefits from treatment in studies of seasonal influenza is strongest when treatment is started within 48 hours of illness onset. However, some benefit, including reduction in mortality or duration of hospitalization, may be seen even for patients whose treatment is started more than 48 hours after illness onset. Recommended duration of treatment is five days.

It is important to remember that seasonal human influenza A strains (both H1 and H3 subtypes) and influenza B continue to circulate in some communities. Seasonal influenza A/H3 and influenza B are sensitive to oseltamivir (Tamiflu) and zanamivir (Relenza). However, seasonal influenza A/H1 is resistant to oseltamivir (Tamiflu). S-OIV is sensitive to oseltamivir (Tamiflu) or zanamivir (Relenza). Recommendations for use of antivirals may change as data on antiviral susceptibilities and effectiveness become available.

Antiviral chemoprophylaxis (pre-exposure or post-exposure) with either oseltamivir or zanamivir is recommended for the following individuals [with reference to A (H1N1) influenza]:

1. Household close contacts of a confirmed or probable case, who are at high-risk for
complications of influenza.
2. Health care workers or public health workers who did not use appropriate personal protective equipment during close contact with an ill confirmed, probable or suspect case of swine-origin influenza A (H1N1) virus infection during the case’s infectious period.

Persons at high risk for complication of influenza include the following:

• persons aged > 50 years of age;
• children < 5 years of age;
• pregnant women;
• persons with chronic diseases such as diabetes mellitus, asthma, heart disease (excluding hypertension), kidney diseases, severe anemia, cancer, and weakened immune systems due to immunosuppressive medications (corticosteroids, anti-TNF alpha medicines, etc.) or HIV infection;
• children aged six months to 18 years who are on long-term aspirin therapy;
• persons with any condition (e.g., cognitive dysfunction, spinal cord injuries, seizure disorders, or other neuromuscular disorders) that can compromise respiratory function or the handling of respiratory secretions or that can increase the risk for aspiration;
• residents of nursing homes and other chronic care facilities

Antiviral chemoprophylaxis with either oseltamivir or zanamivir can be considered for the following:

1. Household close contacts of a suspected case, who are at high-risk for complications of influenza.
2. Children attending school or daycare who are at high-risk for complications of influenza and who had close contact (face-to-face) with a confirmed, probable, or suspected case.
3. Health care workers who are at high-risk for complications of influenza who are working in an area of the healthcare facility that contains patients with confirmed swine-origin influenza A(H1N1) cases.
4. Travelers to Mexico who are at high-risk for complications of influenza.

For Healthcare Providers:

You may consult CDC guidelines for current recommendations for dosing and duration of chemoprophylaxis. These recommendations can be found at http://www.cdc.gov/swineflu/recommendations.htm

Pregnant women should consult their primary provider regarding use of influenza antiviral medications. The CDC has recently issued guidelines for the use of influenza antivirals in pregnancy, which can be found at http://www.cdc.gov/swineflu/clinician_pregnant.htm. The FDA has recently approved oseltamivir (Tamiflu) for treatment and prophylaxis of young children, including infants. Further information on the use of influenza antivirals in young children, including dosing guidelines, can be found at http://www.cdc.gov/swineflu/childrentreatment.htm.

Natural History of Virus

The CDC and CDPH are defining the attack rate and severity of the virus. Please refer to their sites; the

latest molecular studies are fascinating. In brief, the CDC is certain that the severity is not extreme and if

the current patterns are sustained, the severity is likely to be confirmed as mild. The recommendation is

to respond as the usual seasonal influenza.

hi Johnray... good question, others may also wonder.  It is a scenario, perhaps the 'Russians' were used due to the Latest 'pandemic' ...Russian flu- released from cold storage...in the 1970's. .

I found this to be a very interesting read...

Research

1918 Influenza Pandemic Caused by Highly Conserved Viruses with Two Receptor-Binding Variants

Ann H. Reid,* Thomas A. Janczewski,* Raina M. Lourens,* Alex J. Elliot,† Rod S. Daniels,† Colin L. Berry,‡ John S. Oxford,‡§ and Jeffery K. Taubenberger*
*Armed Forces Institute of Pathology, Rockville, Maryland, USA; †National Institute for Medical Research, London, United Kingdom; ‡Queen Mary’s School of Medicine and Dentistry, London, United Kingdom; and §Retroscreen Virology, Ltd., London, United Kingdom

Suggested citation for this article: Reid AH, Janczewski TA, Raina M. Lourens RM, Elliot AJ, Rod S, et al. 1918 Influenza pandemic caused by highly conserved viruses with two receptor-binding variants. Emerg Infect Dis [serial online] 2003 Oct [date cited]. Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no10/02-0789.htm

The Spanish influenza pandemic swept the globe in the autumn and winter of 1918-19, and resulted in the deaths of approximately 40 million people. Clinically, epidemiologically, and pathologically, the disease was remarkably uniform, which suggests that similar viruses were causing disease around the world. To assess the homogeneity of the 1918 pandemic influenza virus, partial hemagglutinin gene sequences have been determined for five cases, including two newly identified samples from London, United Kingdom. The strains show 98.9% to 99.8% nucleotide sequence identity. One of the few differences between the strains maps to the receptor-binding site of hemagglutinin, suggesting that two receptor-binding configurations were co-circulating during the pandemic. The results suggest that in the early stages of an influenza A pandemic, mutations that occur during replication do not become fixed so that a uniform “consensus” strain circulates for some time.

The 1918–19 influenza pandemic began, in some parts of the world, with mild outbreaks in the spring of 1918. In the fall of that year, a lethal wave swept the globe. Outbreaks occurred in early September in North America, Europe, and Africa and spread rapidly, so that the disease had peaked and declined worldwide by the end of December (1–4). Many areas had an additional wave of the disease in the early months of 1919. In most communities, the fall wave of the pandemic lasted approximately l month, with 25% to 30% of the population experiencing symptomatic disease. Clinically, epidemiologically, and pathologically, the disease was remarkably uniform, suggesting that similar viruses were causing disease worldwide (5). To assess the homogeneity of the 1918 pandemic influenza virus, partial hemagglutinin (HA) gene sequences were determined for strains from five cases, including two newly identified samples from London, United Kingdom. The strains show 98.9% to 99.8% nucleotide sequence identity. One of the few differences between the strains maps to the receptor-binding site of HA, which suggests that two receptor-binding configurations were co-circulating during the pandemic.

Influenza A virus is capable of rapid genetic change in mammals (6–8). Its polymerase complex lacks proofreading capability, such that one in five virus particles produced is likely to contain a change at one of its approximately 13,500 nt (9). If such a change provides the virus with a competitive advantage, that strain quickly replaces its predecessor. In humans, the need to escape preexisting immunity exerts positive selection pressure on changes in amino acids comprising the antigenic sites of the surface glycoproteins, HA and neuraminidase (NA) (6,10). The process of progressive change in the antigenic properties of the virus is called antigenic drift and results in the emergence of an antigenically distinct variant strain every 2–3 years. Between drift epidemics, the influenza virus appears to be antigenically uniform (11), but the degree of genetic uniformity has not been studied extensively.

In pandemic influenza, one or both of the virus’s surface proteins are replaced with proteins to which the human population has no preexisting immunity (6,12). The virus then spreads explosively, producing symptomatic infection in up to one third of most populations. During the rapid initial spread of a pandemic strain, little antigenic pressure on the virus exists. One might expect the genetic structure under these circumstances to be relatively constant. However, the degree of genetic identity among viral isolates during a pandemic is not known. Very few full-length HA sequences of viruses from the peaks of the 1957 and 1968 pandemics are available, and all of these viruses had been grown at least once in eggs before sequencing—a process that can select for an unpredictable number of sequence changes (13,14). Therefore, this study represents an initial attempt to measure the degree of genetic homogeneity of a pandemic virus. Since the sequences have been obtained directly from clinical material, they contain no sequence changes attributable to culture.

Materials and Methods

Patients and Samples

The genetic sequences encoding the HA1 domains of three 1918 influenza strains have been determined (15,16). Two of the strains came from U.S. soldiers who died on September 26, 1918: one in Camp Upton, New York, and one in Fort Jackson, South Carolina. The third came from an Inuit woman who died in mid-November 1918 in a remote village on the Seward Peninsula of Alaska.

To obtain further samples for analysis, we examined autopsy material of 14 patients who died in the fall and winter of 1918 to 1919. The material consisted of formalin-fixed, paraffin-embedded tissues, stained slides, and clinical records from the files of the Morbid Anatomy Department of the Royal London Hospital. The cases were preselected by histologic criteria for further analysis, and samples were taken from patients who died from acute influenza after clinical courses of <1 week (16–18). Of these 14 lung samples, 4 were positive for influenza RNA on subsequent molecular genetic analysis, but only 2 had sufficient material for HA1 sequencing. The first patient was a 50-year-old woman admitted to the hospital on November 12, 1918, with influenza and pneumonia. She died on November 13. The postmortem diagnosis was bronchopneumonia. The second patient was a 25-year-old man admitted to the hospital on February 13, 1919. He died on February 15 of influenza. The postmortem diagnosis was lobar pneumonia with toxemia.

Methods

Sample preparation, reverse transcription, polymerase chain reaction (PCR), and sequencing were performed as described previously (15). (Primers used are available upon request.) PCR was performed from at least two separate reverse transcription reactions, and products from at least two PCR reactions were sequenced in each case to ensure accuracy and exclude amplification artifacts. Sequences used to evaluate the complexity of pandemic and epidemic influenza strains were obtained from the Influenza Sequence Database (available from: URL: http://www.flu.lanl.gov/).

Results

The 563-bp fragments sequenced for this study, encoding the antigenic and receptor-binding sites of the HA1 domain (19–21), represent the most variable portion of the influenza genome (Figure). The London cases were designated A/London/1/1918 (H1N1) and A/London/1/1919 (H1N1). These two sequences, when compared to the three previously sequenced North American strains (15), differ from each other by 1 nt to 3 nt, showing a sequence identity of 98.9% to 99.8%.

A/London/1/1918 shows 2 nt differences, compared to A/Brevig Mission/1/1918, one of which would change the amino acid at codon 188 from G to S (amino acid numbering is aligned to the H3 influenza HA). This residue is near several of the residues that have been shown experimentally to affect receptor-binding specificity of H1 HAs (21–23) and next to one of the mapped Sb antigenic site residues (19,20). A/London/1/1919 shows 3 nt differences from A/Brevig Mission/1/1918, 2 of which are nonsynonymous, resulting in changes of V223I and D225G. The V223I change is near Ca antigenic site residues, and the D225G change is at a residue that functions both in receptor-binding and as a Ca antigenic site residue. Amino acid 225 also varies among North American strains; A/New York/1/1918, like A/London/1/1919, has a glycine at position 225, as do most avian influenza strains. A/South Carolina/1/1918 and A/Brevig Mission/1/1918, like A/London/1/1918 and most subsequent human H1 strains, have aspartic acid at this position (Figure) (15). The relative genetic homogeneity of the 1918–19 isolates encouraged us to analyze sequences from the 1957 and 1968 pandemics.

GenBank contains complete HA1 domain–encoding sequences for eight 1957 H2N2 strains. As noted in previous studies of receptor-binding specificity (22,24), the 1957 strains have undergone varying passage histories, but all have been passed at least once. Three of the strains have been sequenced more than once and differ by as many as 8 nt within the same strain. Between sequences, the number of nucleotide differences ranges from only 1 nt difference between A/Chile/6/1957 and A/Davis/1/1957 to 12 differences between one of the A/Japan/305/1957 sequences and one of the A/Singapore/1/1957 sequences. Overall, the sequences show 98.9% to 99.9% identity at the nucleotide level, and 98.5% to 100% identity at the amino acid level.

More limited sequence data are available for the 1968 H3N2 pandemic strains. The complete HA1 domain sequence is available for only three strains, two of which have been sequenced twice each. The two A/NT/60/68/29C sequences differ by 4 nt. The most divergent sequences differ by 24 nt (A/NT/60/68/29C vs. A/Hong Kong/1/68), thus showing 97.6% to 100% identity between sequences at the nucleotide level, and 96.0% to 100% identity at the amino acid level.

Studies from epidemic years have yielded similar results. A 2001 study (25) examined variation in the HA gene of human H3N2 viruses in Spain from 1996 to 2000. During this time, strains antigenically similar to A/Wuhan/359/1995 were replaced by strains similar to A/Sydney/5/1997 and then by strains similar to A/Panama/2007/1999. Within the groups of viruses belonging to each antigenic group, sequence variation was minimal. For example, among the viruses that reacted antigenically with Sydney, but not Panama and Wuhan, 2–10 nt differences occurred over the 591 nt sequenced (98.3% to 99.7% identity).

An unpublished study provides sequences of the HA1 domain of the H3-subtype HA of 16 A/Sydney/05/1997-like (H3N2) influenza virus isolates circulating in Canada during the 1997/98 influenza epidemic season (GenBank no. AF087700–AF087702, AF087707, AF087708, AF096306–AF096316) (26). Two of the isolates had identical sequences, while the others varied by 1 nt to 14 nt over 981 nt (98.6% to 100% identity).

Discussion

The three North American 1918 influenza strains sequenced previously were isolated from patients separated by nearly 2 months in time and almost 4,000 miles in distance (27). Two nucleotide differences were found among these three strains, one of which resulted in an amino acid substitution in the receptor-binding site (15). All three cases likely derived from the initial introduction of the fall wave into the United States, believed to have occurred in Boston in early September 1918. The virus then spread rapidly from Camp Devens, Massachusetts, the first U.S. army base to experience the epidemic, which then reached army bases throughout the eastern United States within 2 weeks (2). Influenza probably reached Brevig Mission, Alaska, via Seattle, Washington. The pandemic reached Camp Lewis, Washington, in mid-September, following the arrival of a troop ship from Philadelphia, Pennsylvania (1,2), and spread to Seattle by late September. After careful screening to exclude sick passengers, a ship left Seattle for Nome, Alaska, in mid-October, but days after its arrival local residents began falling ill (1). An account of the pandemic as it occurred in Brevig Mission reports that visitors from Nome brought the disease to the village in November (28). This chain of events suggests that the Alaskan outbreak was not the result of a separate introduction of the 1918 influenza from Asia to the West Coast of the United States.

The spring wave of the 1918 epidemic was widespread in France and Spain during April and May but did not reach England until June. The fall wave also arrived somewhat later in England than in continental Europe and the United States; peak mortality in London occurred during the first 2 weeks of November (2). A second peak occurred in the third week of February 1919. One strain from each of these peaks was sequenced for this study.

Our results show that strains separated by over 7,500 miles (Brevig Mission, Alaska, to London, United Kingdom) and several months (September 26, 1918, to February 15, 1919) share a sequence identity of 99%. This level of genetic homogeneity is slightly higher than that seen for the available 1957 and 1968 pandemic strains, but the 1957 and 1968 strains were not sequenced directly from clinical material. Sequences from different passages of the same strain were sometimes as different from each other as they were from other strains (29), suggesting that sequence heterogeneity observed was the result of culture adaptation, making it impossible to determine how homogeneous the pandemic viruses actually were. Even so, the 1957 and 1968 pandemic strains show >97% identity between strains. Similar levels of genetic homogeneity were seen in strains from case-patients isolated from a drift epidemic in 1997. Thus, influenza viruses circulating during a single outbreak, whether epidemic or pandemic, show levels of sequence identity consistent with the uniformity of the 1918 cases.

Despite the uniformity of the 1918 strains, one of the variable sites is an amino acid known to be important in receptor binding (21). At a subset of amino acids critical for receptor binding, avian strains differ from swine H1s at only one amino acid, E190D (15). At these amino acids, two of the cases (A/New York/1/1918 and A/London/1/1919) are identical to that of A/sw/Iowa/1976/31 (a classical swine strain). The other 1918 cases have an additional change from the avian consensus at amino acid 225. Since swine viruses with the same receptor site as A/sw/Iowa/1976/31 bind both SAa2,3Gal and SAa2,6Gal (14), A/New York/1/1918 and A/London/1/1919 probably also had the capacity to bind both receptors. Because two of five 1918-19 analyzed fall wave strains from case-patients have the swine-like receptor-binding pattern, the E190D change alone is apparently sufficient to allow viral replication in the human respiratory tract. However, the existence of three strains with the additional G225D change shows that both receptor-binding variants were co-circulating throughout the pandemic. The current evidence does not suggest progression from one receptor-binding pattern to the other during the pandemic, since the two variants are present, on both continents, both early and late in the pandemic. Since residue 225 has also been identified as part of the Ca antigenic site (19), the co-circulating strains possibly differed in antigenic reactivity as well as receptor-binding characteristics.

This study is the first to examine the genetic homogeneity of a pandemic influenza virus directly from clinical material. The results suggest that in the early stages of a pandemic, mutations that occur during replication do not become fixed so that a uniform consensus strain circulates for some time. Studies of influenza strains circulating after 1919 should provide insight into how pandemic viruses evolve after the initial waves through immunologically vulnerable populations. In terms of pandemic planning, our results indicate that a specific antiviral drug or vaccine would have a uniform effect during the important and often lethal first wave of a pandemic (30,31).

This work was supported by a grant from the National Institute of Allergy and Infectious Diseases (R01 AI50619-01) to J.K.T. and by the intramural funds of the Armed Forces Institute of Pathology. J.S.O., C.L.B., and R.S.D. gratefully acknowledge financial support from the Wellcome Trust and the Ian Heap fund.

Ms. Reid is a research biologist in the Molecular Pathology Division at the Armed Forces Institute of Pathology. Her principal research interest is pandemic influenza.

References

1. Crosby A. America’s forgotten pandemic. Cambridge: Cambridge University Press; 1989.
2. Jordan E. Epidemic influenza: a survey. Chicago: American Medical Association; 1927.
3. Reid AH, Taubenberger JK, Fanning TG. The 1918 Spanish influenza: integrating history and biology. Microbes Infect 2001;3:81–7.
4. Taubenberger JK, Reid AH, Janczewski TA, Fanning TG. Integrating historical, clinical and molecular genetic data in order to explain the origin and virulence of the 1918 Spanish influenza virus. Philos Trans R Soc Lond B Biol Sci 2001;356:1829–39.
5. Patterson KD, Pyle GF. The geography and mortality of the 1918 influenza pandemic. Bull Hist Med 1991;65:4–21.
6. Wright PE, Webster RG. Orthomyxoviruses. In: Knipe DM, Howley PM, editors. Fields virology. Vol 1. Philadelphia: Lippincott Williams and Wilkins; 2001:1533–79.
7. Webster RG, Bean WJ, Gorman OT, Chambers TM, Kawaoka Y. Evolution and ecology of influenza A viruses. Microbiol Rev 1992;56:152–79.
8. Lamb RA, Takeda M. Death by influenza virus protein. Nat Med 2001;7:1286–8.
9. Parvin JD, Smith FI, Palese P. Rapid RNA sequencing using double-stranded template DNA, SP6 polymerase, and 3´-deoxynucleotide triphosphates. DNA. 1986;5:167–71.
10. Hay AJ, Gregory V, Douglas AR, Lin YP. The evolution of human influenza viruses. Philos Trans R Soc Lond B Biol Sci 2001;356:1861–70.
11. Centers for Disease Control and Prevention. Influenza summary update: 2001–2 influenza season summary. June 10, 2002. [Accessed September 23, 2002]. Available from: URL: http://www.cdc.gov/ncidod/diseases/flu/weeklyarchives/01-02summary.htm
12. Kilbourne E. Influenza pandemics in perspective. JAMA 1977;237:1225–8.
13. Schild GC, Oxford JS, de Jong JC, Webster RG. Evidence for host-cell selection of influenza virus antigenic variants. Nature 1983;303:706–9.
14. Gambaryan A, Tuzikov A, Piskarev V, Yamnikova SS, Lvov DK, Robertson JS, et al. Specification of receptor-binding phenotypes of influenza virus isolates from different hosts using synthetic sialylglycopolymers: non-egg-adapted human H1 and H3 influenza A and influenza B viruses share a common high binding affinity for 6´-sialyl(N-acetyllactosamine). Virology 1997;232:345–50.
15. Reid AH, Fanning TG, Hultin JV, Taubenberger JK. Origin and evolution of the 1918 “Spanish” influenza virus hemagglutinin gene. Proc Natl Acad Sci U S A 1999;96:1651–6.
16. Taubenberger JK, Reid AH, Krafft AE, Bijwaard KE, Fanning TG. Initial genetic characterization of the 1918 “Spanish” influenza virus [see comments]. Science. 1997;275:1793–6.
17. Winternitz MC, Wason IM, McNamara FP. The pathology of influenza. New Haven (CT): Yale University Press; 1920.
18. Wolbach SB. Comments on the pathology and bacteriology of fatal influenza cases, as observed at Camp Devens, Mass. Johns Hopkins Hospital Bulletin 1919;30:104.
19. Caton AJ, Brownlee GG, Yewdell JW, Gerhard W. The antigenic structure of the influenza virus A/PR/8/34 hemagglutinin (H1 subtype). Cell 1982;31:417–27.
20. Raymond F, Caton A, Cox N, Kendal AP, Brownlee GG. The antigenicity and evolution of influenza H1 haemagglutinin, from 1950–57 and 1977–1983: two pathways from one gene. Virology 1986;148:275–87.
21. Matrosovich M, Gambaryan A, Teneberg S, Piskarev VE, Yamnikova SS, Lvov DK, et al. Avian influenza A viruses differ from human viruses by recognition of sialyloigosaccharides and gangliosides and by a higher conservation of the HA receptor-binding site. Virology 1997;233:224–34.
22. Rogers G, D’Souza B. Receptor binding properties of human and animal H1 influenza virus isolates. Virology 1989;173:317–22.
23. Matrosovich MN, Gambaryan AS, Tuzikov AB, Byramova NE, Mochalova LV, Golbraikh AA, et al. Probing of the receptor-binding sites of the H1 and H3 influenza A and influenza B virus hemagglutinins by synthetic and natural sialosides. Virology 1993;196:111–21.
24. Matrosovich M, Tuzikov A, Bovin N, Gambaryan A, Klimov A, Castrucci MR, et al. Early alterations of the receptor-binding properties of H1, H2, and H3 avian influenza virus hemagglutinins after their introduction into mammals. J Virol 2000;74:8502–12.
25. Coiras MT, Aguilar JC, Galiano M, Carlos S, Gregory V, Lin YP, et al. Rapid molecular analysis of the haemagglutinin gene of human influenza A H3N2 viruses isolated in Spain from 1996 to 2000. Arch Virol 2001;146:2133–47.
26. Macken C, Lu H, Goodman J, Boykin L. The value of a database in surveillance and vaccine selection. In: Osterhaus A, Cox N, Hampson A, editors. Options for the control of influenza IV. Amsterdam: Excerpta Medica; 2001. p. 103–6.
27. Reid AH, Taubenberger JK. The 1918 flu and other influenza pandemics: “over there” and back again. Lab Invest 1999;79:95–101.
28. Fosso C. Alone with death on the Tundra. In: Hedin R, Holthaus G, editors. Alaska: Reflections on land and spirit. Tucscon (AZ): University of Arizona Press; 1989. p. 215–22.
29. Connor R, Kawaoka Y, Webster R, Paulson J. Receptor specificity in human, avian, and equine H2 and H3 influenza virus isolates. Virology 1994;205:17–23.
30. Gensheimer KF, Fukuda K, Brammer L, Cox N, Patriarca PA, Strikes RA. Preparing for pandemic influenza: the need for enhanced surveillance. Vaccine 2002;20(Suppl 2):S63–5.
31. Hayden FG. Perspectives on antiviral use during pandemic influenza. Philos Trans R Soc Lond B Biol Sci 2001;356:1877–84.

 Biochem Biophys Res Commun. 2007 Apr 27;356(1):91-6. Epub 2007 Feb 27. Links

Influenza A viruses of subtypes H1N1 and H3N2 have been reported widely in pigs, associated with clinical disease.

 

From 2005 to 2006, we carried out swine influenza virus surveillance in eight provinces of China. Here we report, for the first time, the isolation and genetic analysis of a human-like influenza H1N1 virus from a pig in a farm of Guangdong province of southern China, a host suspected to generate new pandemic strains through genetic reassortment.

Each of the eight gene segments is of human origin. Phylogenetic analysis indicates that these genes form a human lineage, suggesting that this virus is the descendant of recent human H1N1 influenza viruses.

In addition, four swine H3N2 viruses were also isolated.

Isolation and genetic analysis of human H1N1 and H3N2 influenza viruses from pigs in China provides further evidence about the interspecies transmission of human influenza viruses to pigs and emphasizes the importance of reinforcing swine influenza virus surveillance.

PMID: 17346674 [PubMed - indexed for MEDLINE

source
http://www.ncbi.nlm.nih.gov/pubmed/17346674?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_

DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubm

.

Thank you to LisaP for this site....

Triple-Reassortant Swine Virus Seen Since 2005 in US

NEJM releases content addressing various issues related to outbreak

THURSDAY, May 7 (HealthDay News)

Eleven cases of infection similar to the swine flu outbreak currently under way -- triple-reassortant swine influenza A (H1) viruses -- have been documented since 2005 in the United States, according to a study led by researchers at the U.S. Centers for Disease Control and Prevention in Atlanta and released May 7 by the New England Journal of Medicine. This study was accompanied by another study, two editorials, and three perspectives focused on the swine flu outbreak.

 

The NEJM noted that the swine origin influenza virus (S-OIV) that causes the H1N1 flu is simply the latest strain of H1 hemagglutinin virus which first appeared in both humans and swine in 1918 and has returned in different variants ever since.

 

The S-OIV will continue to mutate in unknown ways over the coming months and might even replace H1 virus as the seasonal flu virus, evolving new antigenic variants every year, the journal speculated. To further support clinicians, who will be challenged to recognize the disease when it returns, the journal said it will establish an H1N1 Influenza Center at NEJM.org to provide information and links to the latest data on the outbreak.

In an editorial, the NEJM urged clinicians to prepare for the next wave of H1N1 flu in the fall and drug manufacturers to launch an accelerated program to develop a vaccine in time.

"Completing seasonal-vaccine production and adding a monovalent S-OIV vaccine to production will be challenging both technically and in terms of policy, but it can be done," the NEJM editorialized.

source
http://www.modernmedicine.com/modernmedicine/Pathology/Triple-Reassortant-Swine-Virus-Seen-Since-2005-in-/ArticleNewsFeed/Article/detail/597185

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H5N1   .... kinda widespread

Did we think it could be ALL OVER the world..... Just not here?

 

http://wildlifedisease.nbii.gov

10/31/07 Saint Clair, MI American black duck Hunter killed  MI Dept of Natural Resources Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

9/29/07 Cascade, MT Mallard Hunter killed  Montana Fish, Wildlife & Parks/USDA Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

6/18/07 Kent, MD Mallard Live birds  USDA/Avian Influenza Coordinated Agricultural Project (AICAP) Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

 

5/21/07 Cape May, NJ Ruddy turnstone Live birds  Southeastern Cooperative Wildlife Disease Study Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

5/10/07 Cape May, NJ Ruddy Turnstone  Live birds  Southeastern Cooperative Wildlife Disease Study Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

10/27/06 Sussex, DE Green-winged teal Hunter killed  USDA/DE Department of Natural Resources Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

10/21/06 Grundy, IL Mallard ducks Hunter killed  USDA/IL Dept of Natural Resources Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

10/19/06 St. Claire, MI Mallard ducks Hunter killed  USDA/MI Dept of Natural Resources Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

8/28/06 Crawford, PA Mallard ducks Live birds  USDA/PA Game Commission Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

8/8/06 Monroe, MI Mute Swans Hunter killed  USDA/MI Dept of Natural Resources Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

8/2/06 Queen Annes, MD Resident wild Mallard ducks Environmental  USDA/Avian Influenza Coordinated Agricultural Project (AICAP) Yes  Yes  Not related to HPAI H5N1; Suspected LPAI H5N1

......................

Genome Analysis

Comparative Sequence Analysis We have compiled multiple sequence alignments and phylogenetic trees for emergent North American H1N1 virus strains. The phylogenetic trees were computed using the HKS + gamma model of evolution with 5 categories. Five categories of strains have been selected for each segment/protein, as follows: a) Current outbreak strains (H1N1, Human): approx. 10 strains distributed by geographic origin as follows: 3 California, 3 Texas, 2 New York, 2-3 Other (Toronto, Germany, New Zealand) b) Approx. 10 H1N1, human, USA, 2007-2008 strains c) Approx. 10 H1N1, swine, USA, 1990-2008 strains d) Approx. 10 H1N1, avian, USA, 1990-2008 strains e) Approx. 5 Hong Kong, swine, H1N1 strains. For categories a, b, and c, that had >10 sequences, strains were selected based on geographic distribution and length. Therefore, shorter sequence with unique locations would be included before longer, duplicate locations. More recent sequences were selected if all other criteria were met. Avian strains (category d) were selected by host species, length, and isolation date (recent isolates). Finally, Hong Kong swine strains (category e) sequences were selected by length and isolation date. In some cases, especially for the polymerase segments, the only sequences in the database were too short to be considered. ←collapse

source for the above

H1N1 (swine flu)

Influenza A

viruses can infect swine, equids, dogs, and other mammalian

species, including humans, however, only birds have been

found to host all of the hemagglutinin and neuraminidase

combinations. The two subtypes which are most important

causes of human influenza are A(H3N2) and A(H1N1), of

which the former is currently associated with the greatest

mortality.

 

source-
The human influenza due to a novel subtype H1N1

ftp://ftp.fao.org/docrep/fao/011/ak061e/ak061e00.pdf
.....................................................................................................................

From: Salient points in the history of swine influenza (adapted from Done and Brown, 1999), from Swine influenza: a zoonosis, Paul Heinen

 

History of swine influenza (In Humans)
...........................................................

 

1918
Swine influenza H1N1 described in north central USA. Hungery, and China.
May have been cause of human pandemic [19], which resulted in 20-40 million
human deaths.

1930
Shope isolated influenza virus from pigs [33], The prototype classic swine
influenza H1N1 strain (A/swinw/Iowa/30) transmitted experimentally to pigs.

1941
Recognized in Europe and disappeared.

1970
Transmission of human H3N2 virus to pigs.  Avian- like H3N2 in pigs in Asia.

1976
Classical H1N1 reappears in European pigs.

1979
Introduction of whole H1N1 virus from birds to pigs. Antigenically distinguishable from classical strains. Still circulating today (2002).

1984
Reassortment between human H3N2 and avian H1N1 in swine resulting in reassortant H3N2 virus with avian
internal gene segments [5]. H3N2 strains first associated with respiratory epizootics. Still circulating today (2002).

1986
Classical H1N1 reappears in UK, similar to classical H1N1 in continental Europe.

1987
Reassortant H3N2 associated with respiratory epizootics in UK. Related to A/Port Chalmers/73 (H3N2).

1989
Avian like swine H1N1 is dominant and widespread in Europe.

1992-1993
Avian like H1N1 strains widespread in UK.

1993
Infection of children with reassortant H3N2 virus from pigs and isolation of avian like swine H1N1 virus from a
pneumonia patient in the Netherlands.

1994
H1N2 first isolated in pigs in UK, and later also in Belgium. Human avian reassortant virus [3, 37].

1992-1998
H3N1 (H3 human, N1 swine) and H1N7 (H1 human, N7 equine) also occurred in swine in the UK but failed to spread.

1998
H9N2 in pigs and humans in Asia [17]. Apparently an avian virus that has adapted to pigs.

1998
For the first time, H3N2 viruses cause severe disease in N. America. Viruses are triple (avian human classical swine) reassortants, distinct from earlier strains and European strains. H1N2 identical to H3N2, but with H1HA from classical swine H1N1, also isolated.

1999
Single case of isolation of avian H4N6 from pigs with pneumonia in Canada.

2002
Current situation in Europe: avian like H1N1, and reassortant human like H3N2 and H1N2. In North America: classical swine H1N1, triple reassortant H3N2.

............................................

it's like multiplication tables. Wash rinse repeat. Repetition is old school learning.

Hey teach   

.

Tamiflu (Oseltamivir) is absolutely  worthless against seasonal influenza (sure hope the Novel Influenza type A doesn't recombinant with it).  If this happens, the only nerominidase inhibitor that would have any effective response would be relenza. Relenza's  (Zanamivir).  method of application is inhaled which gets more of the drug to the source and is more widely effective. (See chart below)  Still has the same side effects but thats the horse I'd bet on.

Unfortunately, we have stockpiled much more Tamiflu than Relenza so don't expect that any would be available.

The best thing you can do if you feel that you are getting the flu is to keep yourself hydrated. Dehydration + flu = a killer.  Vomiting and diarrhea will dehydrate a person very quickly.  Make sure you are drinking 8 glasses of water a day, this won't prevent the flu but you will fair much better if you do come down with it.

Isolates tested (n)	Resistant Viruses, Number (%)		Isolates tested (n)	Resistant Viruses, Number (%)
		Oseltamivir	Zanamivir		Adamantanes
Seasonal Influenza A (H1N1)	865	860 (99.4%)	0 (0)	876	4 (0.5%)
Influenza A (H3N2)	134	0 (0)	0 (0)	145	145 (100%)
Influenza B	424	0 (0)	0 (0)	N/A*	N/A*
Novel Influenza A (H1N1)	101	0 (0)	0 (0)	96	96 (100%)

        ^{*The adamantanes (amantadine and rimantadine) are not effective against influenza B viruses.}

good advice... always wash fruits and veggies before eating.  People handle them in the stores...and this H1N1 can be spread by "soiled hands"

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National News <> @media print { body:before {content: url(http://cleanprint.net/pt/t?&d=2178&p=0&s=NF,NF); } } // cpObject for CleanPrint cpObject={ adPath:'/nationworld_article', adDomain:function(){ var hName = location.hostname; return hName=hName?hName.replace('origin.','www.'):''; }() } // CleanPrint config values var cleanprintConfiguration = { divisionId: '2178', templateId: '3460', tPath: "/fdcp", excludes:['div.articleEmbeddedAdBox','div.articleOptions','div.excludeFromPrint']}; < ="http://extras.mnginteractive.com/live/js/cleanprint/pd.js" =text/ name="cleanprintloader"> Single vaccine likely effective on flu By Karen Kaplan Los Angeles Times Updated: 05/22/2009 11:35:12 PM CDT var requestedWidth = 0; if(requestedWidth > 0){ document.getElementById('articleViewerGroup').style.width = requestedWidth + "px"; document.getElementById('articleViewerGroup').style.margin = "0px 0px 10px 10px"; } A new analysis of more than 50 strains of the H1N1 influenza virus at the center of the global outbreak concludes they are closely related and can be fought with a single vaccine. "We see much less variation among these new H1N1 viruses than we do for typical seasonal influenza viruses," said Dr. Nancy Cox, the senior author of a study released Friday by the journal Science. That will make the job of creating a pandemic flu vaccine "much, much easier," she said. Cox, who heads the influenza division at the Centers for Disease Control and Prevention in Atlanta, and colleagues from the U.S., Mexico and England also found that exposure to the normal seasonal flu strains provides little protection against the novel H1N1 that was identified in April. Those findings could boost the likelihood that the U.S. will move forward with an H1N1 vaccine that would be offered separately from the seasonal flu vaccine. The CDC is testing two potential seed stock candidates for an H1N1 vaccine to see whether they provoke an effective immune response. The candidates combine portions of the H1N1 strain with other flu viruses that are known to grow efficiently in eggs, a key step in the vaccine-making process, Dr. Anne Schuchat, interim deputy director for the CDC's Science and Public Health Program, said Friday. The agency expects to deliver a suitable seed stock to vaccine manufacturers by the end of the month, Schuchat said. In a related development, the Advertisement < = =text/> yld_mgr.place_ad_here("adPosBox"); Department of Health and Human Services announced Friday that it has set aside approximately $1 billion for development of an H1N1 vaccine. Some of the money will fund clinical trials of a vaccine over the summer, and some will be used to ramp up production of key vaccine ingredients in case they are needed, Secretary Kathleen Sebelius said.

I would try to avoid vaccines at most any cost. In 1976, Pres Ford innoculated 40 mil Americans from the flu. More casualties were caused by the vaccine than from illness it was to protect them from.  Earlier this Year Baxter Alexander "accidentally" sent out live H5N1 and a live seasonal strain (H3N9?) virus in flu vaccine to 18 countries. It was discovered by a contractor that tested the vaccine on ferrets, killed em.  The possible recombinics of this combination could have been disastrous (no pun intended).   

Vaccine Ingredients -
Formaldehyde, Aspartame,
Mercury, Etc

 

This following list of common vaccines and their ingredients should shock anyone.   The numbers of microbes, antibiotics, chemicals, heavy metals and animal byproducts is staggering. Would you knowingly inject these materials into your children?   Acel-Immune DTaP - Diphtheria-Tetanus-Pertussis Wyeth-Ayerst 800.934.5556 * diphtheria and tetanus toxoids and acellular pertussis adsorbed, formaldehyde, aluminum hydroxide, aluminum phosphate, thimerosal, and polysorbate 80 (Tween-80) gelatin Act HIB   Haemophilus - Influenza B Connaught Laboratories 800.822.2463 * Haemophilus influenza Type B, polyribosylribitol phosphate ammonium sulfate, formalin, and sucrose   Attenuvax - Measles Merck & Co., Inc. 800-672-6372 * measles live virus neomycin sorbitol hydrolized gelatin, chick embryo   Biavax - Rubella Merck & Co., Inc. 800-672-6372 * rubella live virus neomycin sorbitol hydrolized gelatin, human diploid cells from aborted fetal tissue   BioThrax - Anthrax Adsorbed BioPort Corporation 517.327.1500 * nonencapsulated strain of Bacillus anthracis aluminum hydroxide, benzethonium chloride, and formaldehyde   DPT - Diphtheria-Tetanus-Pertussis GlaxoSmithKline 800.366.8900 x5231 * diphtheria and tetanus toxoids and acellular pertussis adsorbed, formaldehyde, aluminum phosphate, ammonium sulfate, and thimerosal, washed sheep RBCs   Dryvax - Smallpox (not licensed d/t expiration) Wyeth-Ayerst 800.934.5556 * live vaccinia virus, with "some microbial contaminants," according to the Working Group on Civilian Biodefense polymyxcin B sulfate, streptomycin sulfate, chlortetracycline hydrochloride, and neomycin sulfate glycerin, and phenol -a compound obtained by distillation of coal tar vesicle fluid from calf skins Engerix-B   Recombinant Hepatitis B GlaxoSmithKline 800.366.8900 x5231 * genetic sequence of the hepatitis B virus that codes for the surface antigen (HbSAg), cloned into GMO yeast, aluminum hydroxide, and thimerosal   Fluvirin Medeva Pharmaceuticals 888.MEDEVA 716.274.5300 * influenza virus, neomycin, polymyxin, beta-propiolactone, chick embryonic fluid   FluShield Wyeth-Ayerst 800.934.5556 * trivalent influenza virus, types A&B gentamicin sulphate formadehyde, thimerosal, and polysorbate 80 (Tween-80) chick embryonic fluid   Havrix - Hepatitis A GlaxoSmithKline 800.366.8900 x5231 * hepatitis A virus, formalin, aluminum hydroxide, 2-phenoxyethanol, and polysorbate 20 residual MRC5 proteins -human diploid cells from aborted fetal tissue   HiB Titer - Haemophilus Influenza B Wyeth-Ayerst 800.934.5556 * haemophilus influenza B, polyribosylribitol phosphate, yeast, ammonium sulfate, thimerosal, and chemically defined yeast-based medium   Imovax Connaught Laboratories 800.822.2463 * rabies virus adsorbed, neomycin sulfate, phenol, red indicator human albumin, human diploid cells from aborted fetal tissue   IPOL Connaught Laboratories 800.822.2463 * 3 types of polio viruses neomycin, streptomycin, and polymyxin B formaldehyde, and 2-phenoxyethenol continuous line of monkey kidney cells   JE-VAX - Japanese Ancephalitis Aventis Pasteur USA 800.VACCINE * Nakayama-NIH strain of Japanese encephalitis virus, inactivated formaldehyde, polysorbate 80 (Tween-80), and thimerosal mouse serum proteins, and gelatin   LYMErix - Lyme GlaxoSmithKline 888-825-5249 * recombinant protein (OspA) from the outer surface of the spirochete Borrelia burgdorferi kanamycin aluminum hydroxide, 2-phenoxyethenol, phosphate buffered saline   MMR - Measles-Mumps-Rubella Merck & Co., Inc. 800.672.6372 * measles, mumps, rubella live virus, neomycin sorbitol, hydrolized gelatin, chick embryonic fluid, and human diploid cells from aborted fetal tissue   M-R-Vax - Measles-Rubella Merck & Co., Inc. 800.672.6372 * measles, rubella live virus neomycin sorbitol hydrolized gelatin, chick embryonic fluid, and human diploid cells from aborted fetal tissue   Menomune - Meningococcal Connaught Laboratories 800.822.2463 * freeze-dried polysaccharide antigens from Neisseria meningitidis bacteria, thimerosal, and lactose   Meruvax I - Mumps Merck & Co., Inc. 800.672.6372 * mumps live virus neomycin sorbitol hydrolized gelatin   NYVAC - (new smallpox batch, not licensed) Aventis Pasteur USA 800.VACCINE * highly-attenuated vaccinia virus, polymyxcin B, sulfate, streptomycin sulfate, chlortetracycline hydrochloride, and neomycin sulfate glycerin, and phenol -a compound obtained by distillation of coal tar vesicle fluid from calf skins   Orimune - Oral Polio Wyeth-Ayerst 800.934.5556 * 3 types of polio viruses, attenuated neomycin, streptomycin sorbitol monkey kidney cells and calf serum   Pneumovax - Streptococcus Pneumoniae Merck & Co., Inc. 800.672.6372 * capsular polysaccharides from polyvalent (23 types), pneumococcal bacteria, phenol,   Prevnar Pneumococcal - 7-Valent Conjugate Vaccine Wyeth Lederle 800.934.5556 * saccharides from capsular Streptococcus pneumoniae antigens (7 serotypes) individually conjugated to diphtheria CRM 197 protein aluminum phosphate, ammonium sulfate, soy protein, yeast   RabAvert - Rabies Chiron Behring GmbH & Company 510.655.8729 * fixed-virus strain, Flury LEP neomycin, chlortetracycline, and amphotericin B, potassium glutamate, and sucrose human albumin, bovine gelatin and serum "from source countries known to be free of bovine spongioform encephalopathy," and chicken protein   Rabies Vaccine Adsorbed GlaxoSmithKline 800.366.8900 x5231 *rabies virus adsorbed, beta-propiolactone, aluminum phosphate, thimerosal, and phenol, red rhesus monkey fetal lung cells   Recombivax - Recombinant Hepatitis B Merck & Co., Inc. 800.672.6372 * genetic sequence of the hepatitis B virus that codes for the surface antigen (HbSAg), cloned into GMO yeast, aluminum hydroxide, and thimerosal   RotaShield - Oral Tetravalent Rotavirus (recalled) Wyeth-Ayerst 800.934.5556 * 1 rhesus monkey rotavirus, 3 rhesus-human reassortant live viruses neomycin sulfate, amphotericin B potassium monophosphate, potassium diphosphate, sucrose, and monosodium glutamate (MSG) rhesus monkey fetal diploid cells, and bovine fetal serum smallpox (not licensed due to expiration)   40-yr old stuff "found" in Swiftwater, PA freezer Aventis Pasteur USA 800.VACCINE * live vaccinia virus, with "some microbial contaminants," according to the Working Group on Civilian Biodefense polymyxcin B sulfate, streptomycin sulfate, chlortetracycline hydrochloride, and neomycin sulfate glycerin, and phenol -a compound obtained by distillation of coal tar vesicle fluid from calf skins   Smallpox (new, not licensed) Acambis, Inc. 617.494.1339 in partnership with Baxter BioScience * highly-attenuated vaccinia virus, polymyxcin B sulfate, streptomycin sulfate, chlortetracycline hydrochloride, and neomycin sulfate glycerin, and phenol -a compound obtained by distillation of coal tar vesicle fluid from calf skins   TheraCys BCG (intravesicle -not licensed in US for tuberculosis) Aventis Pasteur USA 800.VACCINE * live attenuated strain of Mycobacterium bovis monosodium glutamate (MSG), and polysorbate 80 (Tween-80)   Tripedia - Diphtheria-Tetanus-Pertussis Aventis Pasteur USA 800.VACCINE *Corynebacterium diphtheriae and Clostridium tetani toxoids and acellular Bordetella pertussis adsorbed aluminum potassium sulfate, formaldehyde, thimerosal, and polysorbate 80 (Tween-80) gelatin, bovine extract   US-sourced Typhim Vi - Typhoid Aventis Pasteur USA SA 800.VACCINE * cell surface Vi polysaccharide from Salmonella typhi Ty2 strain, aspartame, phenol, and polydimethylsiloxane (silicone)   Varivax - Chickenpox Merck & Co., Inc. 800.672.6372 * varicella live virus neomycin phosphate, sucrose, and monosodium glutamate (MSG) processed gelatin, fetal bovine serum, guinea pig embryo cells, albumin from human blood, and human diploid cells from aborted fetal tissue   YF-VAX - Yellow Fever Aventis Pasteur USA 800.VACCINE * 17D strain of yellow fever virus sorbitol chick embryo, and gelatin