Published Date: 2009-04-30 23:00:06
Subject: PRO/AH/EDR> Influenza A (H1N1) - worldwide
Archive Number: 20090430.1636

INFLUENZA A (H1N1) - WORLDWIDE
******************************
A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>

[Note: It is now apparent that the 2009 influenza A (H1N1) virus
currently circulating in humans, though genetically linked to swine
influenza viruses, has not been found in swine and that swine do not
appear to be involved in the ongoing epidemic. For that reason, and
in keeping with usage by WHO and other agencies, ProMED will drop the
term "swine flu" from our coverage. We expect the term will continue
to be used by the media and in common usage for some time. - Mod.LM]

In this update:
[1] Origin
[2] Nomenclature
[3] MMWR Dispatch - Drug susceptibility
[4] Clinical questions
[5] Vaccine production
[6] CDC guidance guidance for infection control in healthcare facilities
[7] Interim Guidance for Clinicians

******
[1] Origin
Date: Thu 30 Apr 2009
Source: Eurosurveillance, Vol. 14, issue 17 [edited]
<http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19193>


The origin of the recent swine influenza A(H1N1) virus infecting humans
---------------------------------
By: V Trifonov1, H Khiabanian1, B Greenbaum1,2, R Rabadan 1 At: 1
Department of Biomedical Informatics, Center for Computational
Biology and Bioinformatics, Columbia University College of Physicians
and Surgeons, New York, United States, and 2 The Simons Center for
Systems Biology, Institute for Advanced Study, Princeton, United
States.

Preliminary analysis of the genome of the new H1N1 influenza A virus
responsible for the current pandemic indicates that all genetic
segments are related closest to those of common swine influenza
viruses.

A new H1N1 influenza A virus has been identified in Mexico and has
spread rapidly to other regions around the world. The World Health
Organization in collaboration with many other national and
international agencies is working efficiently to evaluate, diagnose
and implement measures to contain the spread of this virus. Among the
many efforts is the timely release of the genomic sequences from
different viral isolates [1]. This is allowing thousands of
scientists to participate in the endeavor.

There have been some questions raised about the origin of the new
strain. Influenza A is a single stranded RNA virus with 8 different
segments. When 2 viruses co-infect the same cell, new viruses can be
produced that contain segments from both parental strains.

By using sequences collected in public databases, we can identify the
closest relatives of the new strain found in Mexico and construct
clusters and phylogenetic trees. Sequence alignment and similarity,
cluster analyses by principal component analysis and phylogenetic
tree all point to similar results.

Our preliminary analyses show that the closest relatives to this new
strain are found in swine, and occasionally in turkeys. Six segments
of the virus are related to swine viruses from North America and the
other 2 (NA and M) from swine viruses isolated in Europe/Asia. The
closest clusters (for the HA segment) in the NCBI data base are North
America swine influenza A(H1N2) and H3N2s. The closest relatives of
the neuraminidase (NA) gene of the new virus, are influenza A
isolates from 1992. As more data becomes accessible, the evolution of
this gene could be clarified.

The North American ancestors are related to the multiple
reassortants, H1N2 and H3N2 swine viruses isolated in North America
since 1998 [2,3]. In particular, the swine H3N2 isolates from 1998
were a triple reassortment of human, swine and avian origin.

Therefore, this preliminary analysis suggests at least 2 swine
ancestors to the current H1N1, one of them related to the triple
reassortant viruses isolated in North America in 1998. So far, the
new strain has not been reported in pigs. It is not clear whether
this is due to insufficient surveillance of the swine population or
whether this virus has been generated in a very recent reassortment
event.

References
(1) World Health Organization. Viral gene sequences to assist update
diagnostics for swine influenza A(H1N1). Geneva: WHO; 2009 April 25.
Available from:
<http://www.who.int/csr/disease/swineflu/swineflu_genesequences_20090425.pdf >.

(2) Karasin AI, Schutten MM, Cooper LA, Smith CB, Subbarao K,
Anderson GA, et al. Genetic characterization of H3N2 influenza
viruses isolated from pigs in North America, 1977-1999: evidence for
wholly human and reassortant virus genotypes. Virus Res.
2000;68(1):71-85.

(3) Karasin AI, Landgraf J, Swenson S, Erickson G, Goyal S, Woodruff
M, et al. H1N2: Genetic characterization of H1N2 influenza A viruses
isolated from pigs throughout the United States. J Clin Microbiol.
2002;40(3):1073-9.

--
Communicated by:
ProMED-mail <promed@promedmail.org>

******
[2] Nomenclature
Date: Wed 29 Apr 2009
Source: The Bangkok Post, Agence France-Press [edited]
<http://www.bangkokpost.com/breakingnews/141906/us-drops-wine-flu-name>


US drops "swine flu" name
---------------------------
The deadly disease formerly known as "swine flu" is now called the
"2009 H1N1 flu," US officials said Wednesday [29 Apr 2009], as they
battled against a worldwide clampdown on US pork exports. Bidding to
distance the hybrid influenza from pigs, which is responsible for
only one part of the strain, US officials again insisted that people
could not catch H1N1 from eating pork.

The new designation was in the script at briefings by Health and
Human Services Secretary Kathleen Sibelius, Centers for Disease
Control and Prevention acting chief Richard Besser and other US
officials. "We're calling it the 2009 H1N1 flu. That's now the name
for it,'' Besser said.

Pig farmers in the United States, Canada and Mexico -- the disease's
epicenter -- are reeling from bans on their exports of live swine and
pork meat imposed by several nations including Russia and China.
Despite the name swine flu, no pigs in the United States are reported
to be suffering from the disease, which also has components from
influenza strains afflicting people and birds in 3 continents. [More
recent sequence analyses suggest that the 2009 H1N1 influenza virus
is comprised of components derived from 3 different strains of swine
A (H1N1) influenza virus, See ProMED-mail post: Influenza A (H1N1)
"swine flu": worldwide (06). - Mod.CP]

--
Communicated by:
ProMED-mail Rapporteur Mary Marshall

******
[3] MMWR Dispatch - Drug susceptibility
Date: Tue 28 Apr 2009
Source: MMWR Dispatch, Vol. 58 [edited]
<http://www.cdc.gov/mmwr/preview/mmwrhtml/mm58d0428a1.htm?s_cid=mm58d0428a1_e>


Since 21 Apr 2009, CDC has reported cases of respiratory infection
with a swine-origin influenza A (H1N1) virus (S-OIV) that is being
spread via human-to-human transmission (1). As of 28 Apr 2009, the
total number of confirmed S-OIV cases in the United States was 64;
these cases occurred in California (10 cases), Kansas (2), New York
(45), Ohio (one), and Texas (6). The viruses contain a unique
combination of gene segments that had not been reported previously
among swine or human influenza viruses in the United States or
elsewhere (1). Viruses from 13 (20 percent) of 64 patients have been
tested for resistance to antiviral medications. To date, all tested
viruses are resistant to amantadine and rimantadine but are
susceptible to oseltamivir and zanamivir. The purpose of this report
is to provide detailed information on the drug susceptibility of the
newly detected S-OIVs, which will aid in making recommendations for
treatment and prophylaxis for swine influenza A (H1N1) infection.
These data also will contribute to antiviral-resistance monitoring
and diagnostic test development.

Adamantane susceptibility was assessed by conventional sequencing or
pyrosequencing assay (2) with modifications (3), using viral RNA
extracted from original clinical specimens and/or virus isolates.
Susceptibility of virus isolates to the neuraminidase inhibitors
(NAIs), including oseltamivir and zanamivir and 2 investigative NAIs
(peramivir and A-315675), was assessed by chemiluminescent
neuraminidase inhibition assay using the NAStar Kit (Applied
Biosystems, Foster City, California) (4). The generated IC50 values
(i.e., drug concentration needed to inhibit 50 percent of
neuraminidase enzyme activity) of test viruses were compared with
those of sensitive seasonal control viruses. In addition, because
H274Y is the most commonly detected mutation in oseltamivir-resistant
viruses (4,5), a set of new primers for pyrosequencing of the N1 gene
was designed to monitor a residue of the neuraminidase protein at 274
(275 in N1 numbering) in viruses of swine origin (6,7) [These data
are presented as a Table in the original text].

All 13 specimens tested contained the S31N mutation in the M2
protein, which confers cross-resistance to the adamantane class of
anti-influenza drugs [Data presented in a table in the original
text]. In addition, a partial sequence deduced from the M2 pyrograms
revealed changes characteristic for the M gene of S-OIVs. Existing
primers used for the detection of adamantane resistance in seasonal
viruses do not work with all tested S-OIVs. Optimized primers have
been designed and are currently being validated. All 13 tested virus
isolates exhibited IC50 values characteristic of oseltamivir- and
zanamivir-sensitive influenza viruses. A/Georgia/17/2006 (H1N1),
which is a seasonal virus, was used as a control. The IC50 for
oseltamivir ranged from 0.28 nM to 1.41 nM, whereas those for
zanamivir ranged from 0.30 nM to 1.34 nM. All tested viruses also
were susceptible to peramivir and A-315675. A subset of viruses (n=2)
tested in the fluorescent neuraminidase inhibition assay showed IC50
for oseltamivir and zanamivir ranging from 1.50 nM to 2.40 nM,
similar to the sensitive control. Among the 36 specimens tested to
date with pyrosequencing for the H274Y mutation in N1, none had
mutations at residue 274.

[Reported by: L Gubareva, PhD, M Okomo-Adhiambo, PhD, V Deyde, PhD,
AM Fry, MD, TG Sheu, R Garten, PhD, C Smith, J Barnes, A Myrick, M
Hillman, M Shaw, PhD, C Bridges, MD, A Klimov, PhD, N Cox, PhD,
Influenza Div, National Center for Infectious and Respiratory
Diseases, Coordinating Center for Infectious Diseases, CDC]

MMWR Editorial Note:
In the United States, 2 classes of antiviral drugs are approved by
the Food and Drug Administration (FDA) for use in treating or
preventing influenza virus infections: M2 ion channel blockers and
NAIs. The M2 blockers (adamantanes) are effective against influenza A
viruses but not influenza B viruses, which lack the M2 protein (8).
However, use of the M2 blockers has been associated with the rapid
emergence of drug-resistance mutations of the M2 protein among human
influenza A viruses of H3N2 subtype, and in H1N1 subtype viruses
circulating in certain geographic areas (2,3,9). Adamantane
resistance also has been detected in A (H5N1) viruses in Southeast
Asia (10,11). In addition, adamantane resistance has been reported
for swine viruses in Eurasia (12-14) but not in North America. This
rapid increase in resistance has reduced the usefulness of this class
of drugs for the management of influenza A infections, and since
2005, CDC has not recommended their use (15), although the emergence
of resistance to oseltamivir in seasonal influenza viruses
circulating during the 2008-09 season led to changes in CDC
recommendations.*

Two NAIs, oseltamivir (Tamiflu [Hoffman-La Roche, Ltd, Basel,
Switzerland]) and zanamivir (Relenza [GlaxoSmithKline, Stevenage,
United Kingdom]) are FDA-approved drugs for use against type A and
type B influenza infections (16). The 2 drugs differ structurally,
resulting in oseltamivir being orally bioavailable, whereas zanamivir
is not and must be inhaled (17,18). A 3rd NAI, peramivir (BioCryst,
Inc., Birmingham, Alabama), is formulated for intravenous
administration and is undergoing clinical trials, and a 4th, called
A-315675 (Abbott Laboratories, Abbott Park, Illinois) has only been
investigated in preclinical studies.

Compared with M2 blockers, NAIs previously exhibited lower frequency
of antiviral resistance during therapeutic use (16,19). However,
during the 2007-08 influenza season, emergence and transmission of
oseltamivir-resistant A (H1N1) viruses, with a H274Y mutation in the
neuraminidase protein, was simultaneously detected in several
countries in the Northern Hemisphere (4,20-22) and spread globally
(7,9,23). As of April 2009, similar trends have been observed in the
2008-09 influenza season, with many countries reporting up to 100
percent oseltamivir resistance in A (H1N1) viruses. As a result, the
World Health Organization Global Influenza Surveillance Network
(GISN) and CDC have emphasized the urgent need for close monitoring
of resistance to NAIs. Current interim antiviral recommendations for
treatment and chemoprophylaxis of swine influenza A (H1N1) viruses
include the use of either zanamivir or oseltamivir and are available
at
<http://www.cdc.gov/swineflu/recommendations.htm>.

References:
(1) CDC. Swine influenza A (H1N1) infection in 2 children---southern
California, March--April 2009. MMWR 2009;58:400--2.
(2) Bright RA, Medina MJ, Xu X, et al. Incidence of adamantane
resistance among influenza A (H3N2) viruses isolated worldwide from
1994 to 2005: a cause for concern. Lancet 2005;366:1175--81.
(3) Deyde VM, Xu X, Bright RA, et al. Surveillance of resistance to
adamantanes among influenza A (H3N2) and A (H1N1) viruses isolated
worldwide. J Infect Dis 2007;196:249--57.
(4) Sheu TG, Deyde VM, Okomo-Adhiambo M, et al. Surveillance for
neuraminidase inhibitor resistance among human influenza A and B
viruses circulating worldwide in 2004--2008. Antimicrob Agents
Chemother 2008;52:3284--92.
(5) Lackenby A, Hungnes O, Dudman SG, et al. Emergence of resistance
to oseltamivir among influenza A (H1N1) viruses in Europe. Euro
Surveill 2008;13(5).
(6) Deyde VM, Okomo-Adhiambo M, Sheu TG, et al. Pyrosequencing as a
tool to detect molecular markers of resistance to neuraminidase
inhibitors in seasonal influenza A viruses. Antiviral Res
2009;81:16--24.
(7) Lackenby A, Democratis J, Siqueira MM, Zambon MC. Rapid
quantitation of neuraminidase inhibitor drug resistance in influenza
virus quasispecies. Antivir Ther 2008;13:809--20.
(8) Hayden FG. Adamantadine and rimantadine---clinical aspects. In:
DD Richman, ed. Antiviral drug resistance. San Francisco, CA: John
Wiley and Sons Ltd.; 1996:59--77.
(9) CDC. Influenza activity---United States and worldwide, 2007--08
season. MMWR 2008;57:692--7.
(10) He G, Qiao J, Dong C, He C, Zhao L, Tian Y.
Amantadine-resistance among H5N1 avian influenza viruses isolated in
northern China. Antiviral Res 2008;77:72--6.
(11) Cheung CL, Rayner JM, Smith GJ, et al. Distribution of
amantadine- resistant H5N1 avian influenza variants in Asia. J Infect
Dis 2006;193:1626--9.
(12) Krumbholz A, Schmidtke M, Bergmann S, et al. High prevalence of
amantadine resistance among circulating European porcine influenza A
viruses. J Gen Virol 2009;90(Pt 4):900--8.
(13) Schmidtke M, Zell R, Bauer K, et al. Amantadine resistance among
porcine H1N1, H1N2, and H3N2 influenza A viruses isolated in Germany
between 1981 and 2001. Intervirology 2006;49:286--93.
(14) Gregory V, Lim W, Cameron K, et al. Infection of a child in Hong
Kong by an influenza A H3N2 virus closely related to viruses
circulating in European pigs. J Gen Virol 2001;82(Pt 6):1397--406.
(15) Bright RA, Shay DK, Shu B, Cox NJ, Klimov AI. Adamantane
resistance among influenza A viruses isolated early during the
2005--2006 influenza season in the United States. JAMA
2006;295:891--4.
(16) Moscona A. Neuraminidase inhibitors for influenza. N Engl J Med
2005;353:1363--73.
(17) Smith BJ, McKimm-Breshkin JL, McDonald M, Fernley RT, Varghese
JN, Colman PM. Structural studies of the resistance of influenza
virus neuramindase to inhibitors. J Med Chem 2002;45:2207--12.
(18) Colman PM. Zanamivir: an influenza virus neuraminidase
inhibitor. Expert Rev Anti Infect Ther 2005;3:191--9.
(19) Monto AS, McKimm-Breschkin JL, Macken C, et al. Detection of
influenza viruses resistant to neuraminidase inhibitors in global
surveillance during the 1st 3 years of their use. Antimicrob Agents
Chemother 2006;50:2395--402.
(20) Dharan NJ, Gubareva LV, Meyer JJ, et al. Infections with
oseltamivir-resistant influenza A (H1N1) virus in the United States.
JAMA 2009;301:1034--41.
(21) Hauge SH, Dudman S, Borgen K, Lackenby A, Hungnes O.
Oseltamivir- resistant influenza viruses A (H1N1), Norway, 2007--08.
Emerg Infect Dis 2009;15:155--62.
(22) Meijer A, Lackenby A, Hungnes O, et al. Oseltamivir-resistant
influenza virus A (H1N1), Europe, 2007--08 season. Emerg Infect Dis
2009;15:552--60.
(23) Besselaar TG, Naidoo D, Buys A, et al. Widespread oseltamivir
resistance in influenza A viruses (H1N1), South Africa. Emerg Infect
Dis 2008;14:1809--10.

--
Communicated by:
ProMED-mail <promed@promedmail.org>

******
[4] Clinical questions
Date: Wed 29 Apr 2009
From: Andre Dascal <andre.dascal@mcgill.ca>


This email is addressed to clinicians or public health physicians who
have cared for or have knowledge of the clinical presentation of the
present swine influenza cases.

We are interested in age specific frequency of symptoms and signs of
patients with confirmed swine flu. In addition, we would like to know
whether any in the age range of 16 to 64 have been confirmed and had
no fever and/or no cough prior to viral testing.

We are aware that fever is part of the present case definition, thus
probably most if not all probably have had fever. However, we wonder
whether any were tested even though no fever was present.

We also wonder how many had cough vs. other respiratory manifestations.

--
Andre Dascal MD, FRCPC
Associate Professor of Medicine, Microbiology and Immunology,
McGill University
<andre.dascal@mcgill.ca>

[Any reader able to provide the information requested by Dr Andre
Dascal should contact him directly. - Mod.CP]

******
[5] Vaccine production
Date: Wed 29 Apr 2009
Source: Scientific American, 60 Second Science [edited]
<http://www.sciam.com/blog/60-second-science/post.cfm?id=vaccine-makers-await-critical-swine-2009-04-29>


As the World Health Organization (WHO) today [29 Apr 2009]
acknowledged the spreading swine influenza virus by moving the
pandemic threat awareness level up one notch to 5, the U.S. Centers
for Disease Control (CDC) worked to get drug companies the materials
they need to create a vaccine. Meanwhile, the U.S. Department of
Health and Human Services (HHS) said it is unlikely that any new
swine flu vaccine would be included in the batches of seasonal
influenza vaccines already in production for the typical August
vaccine ship date.

CDC and others are working to create the virus reference strain by
the end of May 2009 that drug companies need to make a vaccine, says
Bruce Gellin, Director of HHS's National Vaccine Program Office and
the agency's deputy assistant secretary for health. Once these
companies make the necessary adjustments to their facilities and
processes (which usually takes 2 or more weeks), he adds, they begin
developing a pilot vaccine that the National Institutes of Health
(NIH) tests to determine the amount of antigen per dose and number of
doses, as well as information on safety.

"For a number of reasons, it is unlikely that [a swine flu vaccine]
will be included in the seasonal vaccine," Gellin says. "As the
seasonal vaccine is currently in the final phases of production,
waiting for this additional strain would delay the availability of
seasonal vaccine."

In addition, if the new vaccine requires 2 doses, it would complicate
use of the seasonal vaccine, as most (except children vaccinated for
the 1st time) require only a single dose each year. "We may learn
something from the clinical trials," he adds, "but the assumption
going in is that a new virus that's not been seen in people before
will require 2 doses."

Pharmaceuticals manufacturer Sanofi Pasteur, based in Lyon, France,
agrees that the fastest and safest way to proceed is to maintain 2
separate vaccines for swine flu and for seasonal flu. "Production of
the seasonal vaccine is well underway," company spokesperson Donna
Cary says, confirming that attempts to combine vaccines would delay
the seasonal vaccine.

While the extent of the current swine flu spread is yet to be seen,
she adds, "we do know that seasonal influenza hospitalizes 200 000
people annually and resulted in about 36 000 deaths (in the U.S.)
this year [2009]." The WHO and CDC meet in January each year to
determine which influenza strains to include in that year's vaccine,
which drug makers typically begin shipping in August.

Biotech firm Novavax, Inc. in Rockville, Md., is one of the few drug
makers not waiting for the CDC to provide a live strain of the H1N1
virus. Instead, the company has begun developing a prototype swine
flu vaccine using information the CDC has posted to the Global
Initiative on Sharing Avian Influenza Data (GISAID) database,
launched in 2006 by a number of science institutes and universities
worldwide (including the WHO, CDC and Max-Planck-Institute for
Informatics) to encourage data-sharing in response to the global
spread of the H5N1 avian flu.

"The clock started last week on Friday [24 Apr 2009]," says Gale
Smith, vice president of vaccine development for Novavax, which has
seasonal flu vaccines in late-stage clinical testing but no products
currently on the market. Novavax claims to have developed a
virus-like particle (VLP) technology that allows the company to
manufacture a vaccine to match a particular virus strain in about 3
months. The recombinant VLPs, created without the use of any genetic
material, contain surface proteins that make the particles look like
a virus and can elicit an immune response, even though they lack the
genes needed to replicate themselves.

Despite being a relative newcomer with a largely untested technique,
Novavax is hoping to create a vaccine that could be given emergency
approval for use by first responders, if no other vaccines are
available, Smith says. The company plans to have a prototype vaccine
to show the CDC or HHS within 3 months. Novavax's seasonal flu
vaccine is currently in Phase III trials for efficacy and safety, but
it could be years before that vaccine receives FDA approval.

As the vaccine makers await the materials needed get their products
off the ground, London-based GlaxoSmithKline is ramping up production
of its antiviral drug Relenza (zanamivir). Lab testing on oseltamivir
(Tamiflu) and zanamivir indicates they could be up to 90 percent
effective in staving off the current swine flu virus, according to
the CDC <http://www.cdc.gov/swineflu/antiviral_swine.htm>.
The swine influenza A (H1N1) viruses found in humans over the past
week are resistant to the other 2 anti-influenza drugs on the market,
amantadine (Symmetrel) and rimantadine (Flumadine).

[Byline: Larry Greenemeier]

--
Communicated by:
ProMED-mail <promed@promedmail.org>

******
[6] CDC guidance guidance for infection control in healthcare facilities
Date: Wed 29 Apr 2009
Source: CDC
<http://www.cdc.gov/swineflu/guidelines_infection_control.htm>

Interim Guidance for Infection Control for Care of Patients with
Confirmed or Suspected Swine Influenza A (H1N1) Virus Infection in a
Healthcare Setting

This document provides interim guidance for healthcare facilities
(e.g., hospitals, long-term care and outpatient facilities, and other
settings where healthcare is provided) and will be updated as needed.

[The full guidance can be found at the above URL. - Mod.LM]
--
Communicated by:
ProMED-mail Rapporteur Brent Barrett

******
[7] Interim Guidance for Clinicians
Date: Wed 29 Apr 2009
Source: CDC
<http://www.cdc.gov/swineflu/identifyingpatients.htm>

Interim Guidance for Clinicians on Identifying and Caring for
Patients with Swine-origin Influenza A (H1N1) Virus Infection

This document provides interim guidance for clinicians who might
provide care for patients with swine-origin influenza A (H1N1) or
suspected
swine-origin influenza A (H1N1) virus infection. It will be
periodically updated as information becomes available.

[The full guidance can be found at the above URL. - Mod.LM]
--
Communicated by:
ProMED-mail Rapporteur Brent Barrett


[see also;
Influenza A (H1N1) "swine flu": worldwide (07), update, pandemic 5
20090429.1622
Influenza A (H1N1) "swine flu": worldwide (06) 20090429.1614
Influenza A (H1N1) "swine flu": worldwide (05) 20090428.1609
Influenza A (H1N1) "swine flu": worldwide (04) 20090428.1601
Influenza A (H1N1) "swine flu": worldwide (03) 20090428.1600
Influenza A (H1N1) "swine flu": Worldwide (02) 20090427.1586
Influenza A (H1N1) "swine flu": Worldwide 20090427.1583
Influenza A (H1N1) virus, human: worldwide 20090426.1577
Influenza A (H1N1) virus, human - New Zealand, susp 20090426.1574
Influenza A (H1N1) virus, human - N America (04) 20090426.1569
Influenza A (H1N1) virus, human - N America (03) 20090426.1566
Influenza A (H1N1) virus, human - N America (02) 20090425.1557
Influenza A (H1N1) virus, human - N America 20090425.1552
Acute respiratory disease - Mexico, swine virus susp 20090424.1546
Influenza A (H1N1) virus, swine, human - USA (02): (CA, TX) 20090424.1541
Influenza A (H1N1) virus, swine, human - USA: (CA) 20090422.1516
Influenza A (H1N1) virus, swine, human - Spain 20090220.0715
2008
----
Influenza A (H1N1) virus, swine, human - USA (TX) 20081125.3715
2007
----
Influenza A (H2N3) virus, swine - USA 20071219.4079
Influenza, swine, human - USA (IA): November 2006 20070108.0077]
................................................cp/msp/lm

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