During May 21–September 23, 2017,* the United States experienced low-level seasonal
influenza virus activity; however, beginning in early September, CDC received reports
of a small number of localized influenza outbreaks caused by influenza A(H3N2) viruses.
In addition to influenza A(H3N2) viruses, influenza A(H1N1)pdm09 and influenza B viruses
were detected during May–September worldwide and in the United States. Influenza B
viruses predominated in the United States from late May through late June, and influenza
A viruses predominated beginning in early July. The majority of the influenza viruses
collected and received from the United States and other countries during that time
have been characterized genetically or antigenically as being similar to the 2017
Southern Hemisphere and 2017–18 Northern Hemisphere cell-grown vaccine reference viruses;
however, a smaller proportion of the circulating A(H3N2) viruses showed similarity
to the egg-grown A(H3N2) vaccine reference virus which represents the A(H3N2) viruses
used for the majority of vaccine production in the United States. Also, during May
21–September 23, 2017, CDC confirmed a total of 33 influenza variant virus
†
infections; two were influenza A(H1N2) variant (H1N2v) viruses (Ohio) and 31 were
influenza A(H3N2) variant (H3N2v) viruses (Delaware [1], Maryland [13], North Dakota
[1], Pennsylvania [1], and Ohio [15]). An additional 18 specimens from Maryland have
tested presumptive positive for H3v and further analysis is being conducted at CDC.
United States
The U.S. Influenza Surveillance System
§
is a collaboration between CDC and federal, state, local, and territorial partners
and uses eight data sources to collect influenza information,
¶
six of which operate year-round. U.S. World Health Organization (WHO) and National
Respiratory and Enteric Virus Surveillance System laboratories, which include both
public health and clinical laboratories throughout the United States, contribute to
virologic surveillance for influenza. During May 21–September 23, 2017, clinical laboratories
in the United States tested 153,397 respiratory specimens for influenza viruses, 3,785
(2.5%) of which were positive (Figure 1). Among these, 1,885 (49.8%) were positive
for influenza A viruses, and 1,900 (50.2%) were positive for influenza B viruses.
Public health laboratories in the United States tested 6,431 respiratory specimens
collected during May 21–September 23, 2017. Among these, 1,536 were positive for influenza
(Figure 2), including 842 (54.8%) that were positive for influenza A viruses, and
694 (45.2%) that were positive for influenza B viruses. Influenza B viruses were more
commonly reported from late May through late June, and influenza A viruses have predominated
since early July. Among the 828 (98.3%) influenza A viruses subtyped by public health
laboratories, 715 (86.4%) were influenza A(H3N2) and 113 (13.6%) were influenza A(H1N1)pdm09
virus. Among the 537 (77.4%) influenza B viruses for which lineage was determined,
398 (74.1%) belonged to the B/Yamagata lineage and 139 (25.9%) belonged to the B/Victoria
lineage.
FIGURE 1
Number* and percentage of respiratory specimens testing positive for influenza reported
by clinical laboratories, by influenza virus type and surveillance week — United States,
October 2, 2016–September 23, 2017
†
* 131,519 (12.3%) of 1,067,211 tested were positive during October 2, 2016–September
23, 2017.
† As of September 29, 2017.
The figure above is a combination line graph and bar chart showing the number and
percentage of respiratory specimens testing positive for influenza reported by clinical
laboratories, by influenza virus type and surveillance week in the United States during
October 2, 2016–September 23, 2017.
FIGURE 2
Number* of respiratory specimens testing positive for influenza reported by public
health laboratories, by influenza virus type, subtype/lineage, and surveillance week
— United States, October 2, 2016–September 23, 2017
†
* N = 42,875.
† As of September 29, 2017.
The figure above is a bar chart showing the number of respiratory specimens testing
positive for influenza reported by public health laboratories, by influenza virus
type, subtype/lineage, and surveillance week in the United States during October 2,
2016–September 23, 2017.
During May 21–September 23, the weekly percentage of outpatient visits to health care
providers for influenza-like illness** from the U.S. Outpatient Influenza-Like Illness
Surveillance Network remained below the national baseline
††
of 2.2%, ranging from 0.7% to 1.2%. Based on data from CDC’s National Center for Health
Statistics Mortality Surveillance System, the percentage of deaths attributed to pneumonia
and influenza did not exceed the epidemic threshold
§§
and ranged from 5.1% to 6.1%. Four influenza-associated pediatric deaths occurring
during May 21–September 23 were reported; two were associated with an influenza A(H3N2)
virus, one was associated with an influenza A(H1N1)pdm09 virus, and one was associated
with an influenza B virus.
Novel Influenza A Virus Infections
Fifty-one human infections with novel influenza A viruses were reported in the United
States during May 21–September 23, 2017. All of these were variant virus infections
(human infections with influenza viruses that normally circulate in swine). Thirty-one
have been sequenced and are H3N2v viruses reported from five states (Delaware [1],
Maryland [13], North Dakota [1], Pennsylvania [1], and Ohio [15]) and two were H1N2v
viruses, both from Ohio. The remaining 18 viruses have tested presumptive positive
for H3v at the Maryland public health laboratory and further confirmatory testing
is being performed by CDC. All 51 patients reported exposure to swine in a fair setting
during the week preceding illness onset. Swine influenza A viruses were identified
from respiratory specimens collected from pigs at multiple fairs. Forty-seven of the
51 patients were children aged <18 years and four patients were adults aged ≥50 years.
Three of the 51 patients were hospitalized. All other patients are recovering or have
fully recovered from their illness. No human-to-human transmission of these viruses
has been identified.
The viruses detected in Maryland, Ohio, North Dakota, and Pennsylvania all had a hemagglutinin
(HA) gene derived from a seasonal human H3N2 virus that was likely introduced into
swine by reverse zoonosis (i.e., humans infecting swine) in 2010. These viruses were
closely related to H3N2 viruses known to circulate in the U.S. swine population, as
well as to variant virus infections detected in Ohio and Michigan during 2016 (
1
). Further analysis of the variant viruses detected in the most recent cases from
Maryland is being performed at CDC. One of the H1N2v viruses had an HA gene from the
alpha sublineage of the classical swine H1 HA lineage (
2
). This is the second alpha sublineage H1N2v virus detected since the mid-1990s. The
second H1N2v virus had an HA gene representative of the delta 2 sublineage circulating
in swine. The HA and neuraminidase (NA) genes are closely related to 2016/2017 swine
influenza viruses from the United States. The NA genes of both H3N2v and H1N2v viruses
are related to human H3N2 viruses that likely entered the North American swine population
around 2002 and have remained the predominant NA found in contemporary swine influenza
viruses.
Worldwide
CDC serves as a WHO Collaborating Center for Surveillance, Epidemiology, and Control
of Influenza, one of six WHO Collaborating Centers for Influenza in the WHO Global
Influenza Surveillance and Response System (GISRS).
¶¶
CDC, along with other international public health partners, provides surveillance
and virus characterization data to WHO.*** The timing of influenza activity around
the world varies by region,
†††
and areas with similar influenza transmission patterns are grouped by influenza transmission
zones.
§§§
Reports from GISRS during May 21–September 23 suggested that typical seasonal patterns
of influenza activity occurred in temperate climate Southern Hemisphere countries
(
3
). Influenza activity began to increase in late April in the temperate countries of
South America, late May in Southern Africa, early June in New Zealand, and early July
in Australia. Influenza activity peaked in mid-June in temperate South America, the
beginning of July in Southern Africa and New Zealand, and in mid-August in Australia,
although elevated activity continued through September in Southern Africa and Australia.
Influenza A(H3N2) viruses predominated across the Southern Hemisphere countries, with
some reported influenza B viruses cocirculating in temperate South America, New Zealand,
and Australia. In temperate-climate countries of Europe and North America, influenza
activity was low, with influenza B viruses predominating.
In countries with tropical influenza seasonality, influenza activity levels and the
predominant virus varied by country. In Central America and the Caribbean, activity
was low and influenza A(H3N2) and influenza B viruses predominated. In tropical South
America, influenza activity decreased from May 21 through September 23; influenza
A(H3N2) viruses predominated with some influenza B viruses reported. Sporadic influenza
virus detections were reported in Eastern and Western Africa, with influenza A(H1N1)pdm09,
influenza A(H3N2), and influenza B viruses cocirculating. In Eastern Asia, high levels
of influenza activity were reported in Southern China, Hong Kong special administrative
region (SAR), and Taiwan beginning in July, peaked in mid-August, and decreased through
September 23; influenza A(H3N2) viruses predominated. In Southern Asia, influenza
A(H1N1)pdm09 viruses predominated, with elevated activity reported in India, Nepal,
and the Maldives. Influenza activity in Southeast Asia was elevated in August and
September. Influenza A(H1N1)pdm09 viruses predominated in the Philippines and Myanmar.
Influenza A(H3N2), influenza A(H1N1)pdm09, and influenza B viruses cocirculated in
Singapore, and influenza A(H1N1)pdm09 and influenza B viruses cocirculated in Vietnam.
During May 23–September 13, WHO reported 100 laboratory-confirmed human infections
with avian influenza viruses, all from China, including 99 Asian lineage avian influenza
A(H7N9) infections, and one influenza A(H9N2) infection.
¶¶¶
A total of 764 human infections, including 283 (37%) deaths, with Asian lineage avian
influenza A(H7N9) virus were reported to WHO from more provinces, regions, and municipalities
in China during the fifth epidemic than in the previous four epidemics combined (
4
).
Genetic and Antigenic Characterization of Influenza Viruses
The 2017–18 influenza vaccine virus components were selected in March 2017, during
one of two biannual WHO-sponsored vaccine consultation meetings to review influenza
data generated by GISRS laboratories. The recommended Northern Hemisphere 2017–18
trivalent influenza vaccine composition consists of an A/Michigan/45/2015 (H1N1)pdm09-like
virus, an A/Hong Kong/4801/2014 (H3N2)-like virus, and a B/Brisbane/60/2008-like (B/Victoria
lineage) virus. An additional influenza B virus (B/Phuket/3073/2013-like [B/Yamagata
lineage]) was recommended for quadrivalent vaccines.**** These recommendations reflect
an update to the A(H1N1)pdm09 virus component to a more contemporary influenza A(H1N1)pdm09
virus (an A/California/7/2009 (H1N1)pdm09-like virus was replaced with an A/Michigan/45/2015
(H1N1)pdm09-like virus), compared with the recommendation for the Northern Hemisphere
2016–2017 influenza season and are the same as the vaccine virus recommendations made
for the 2017 Southern Hemisphere influenza vaccine.
Most influenza vaccines licensed in the United States, with the exception of cell
culture–based inactivated influenza vaccine (ccIIV4) and recombinant influenza vaccines
(RIV3 and RIV4) are produced through propagation of candidate vaccine viruses (CVVs)
in eggs. Historically, CVVs provided to manufacturers have been egg-derived. Egg propagation
of influenza viruses, particularly influenza A(H3N2) viruses, often leads to genetic
changes that might have antigenic implications. The vaccine viruses selected for the
Northern Hemisphere 2017–18 vaccine were representative of most, but not all, circulating
influenza viruses at that time, and had the fewest and least substantial egg-adapted
changes. In August 2016, the Food and Drug Administration approved the use of cell-derived
CVVs for inclusion in ccIIV4.
††††
For the 2017–18 season, the influenza A(H3N2) component of this vaccine is manufactured
using a cell-derived CVV. The other components of this vaccine are manufactured using
egg-derived CVVs. Production of influenza vaccines using cell-grown CVVs and cell-based
technology can circumvent antigenic changes that might be associated with egg propagation,
particularly for influenza A(H3N2) viruses.
§§§§
Data obtained from antigenic characterization are important in the assessment of the
similarity between reference vaccine viruses and circulating viruses. In vitro antigenic
characterization data acquired through hemagglutination inhibition (HI) assays or
virus neutralization assays are used to assess whether genetic changes in circulating
viruses affect antigenicity, which could affect vaccine effectiveness. Since the 2014–15
season, many influenza A(H3N2) viruses lack sufficient hemagglutination titers for
antigenic characterization using hemagglutination inhibition assays. Therefore, representative
influenza A(H3N2) viruses are selected for antigenic characterization using the virus
neutralization focus reduction assay to assess the ability of various antisera to
neutralize infectivity of the test viruses. For nearly all influenza-positive surveillance
samples received by CDC, next generation sequencing (NGS), which employs genomic enrichment
practices (
5
–
7
), adapted by CDC, Nextera library preparation (Illumina, San Diego, California) and
NGS using MiSeq (Illumina, San Diego, California), is performed to determine the genetic
identity of circulating viruses. The genomic data are analyzed and submitted to public
databases (GenBank or GISAID EpiFlu). CDC has antigenically or genetically characterized
877 influenza viruses collected and submitted by U.S. and international laboratories
since May 21, 2017, including 117 influenza A(H1N1)pdm09 viruses, 495 influenza A(H3N2)
viruses, and 265 influenza B viruses.
Phylogenetic analysis of the HA genes from the A(H1N1)pdm09 viruses collected since
May 21, 2017, showed that all but one were in subclade 6B.1, and one virus belonged
to clade 6B (Figure 3). All A(H1N1)pdm09 viruses were antigenically similar (analyzed
using HI with ferret antisera) to the 6B.1 virus A/Michigan/45/2015, the recommended
influenza A(H1N1)pdm09 reference virus for the 2017 Southern Hemisphere and 2017–18
Northern Hemisphere influenza vaccines.
FIGURE 3
Genetic characterization of U.S. and international viruses collected during May 21,
2017–September 23, 2017*
* As of September 29, 2017.
The figure above is a bar chart showing the genetic characterization of U.S. and international
viruses collected during May 21, 2017–September 23, 2017.
Four hundred ninety-five influenza A(H3N2) viruses collected globally since May 21,
2017, were sequenced, and phylogenetic analysis of the HA genes illustrated that multiple
clades/subclades were cocirculating (Figure 3). The HA genes showed extensive diversity
and belonged to clades 3C.2a or 3C.3a, with 3C.2a predominating (Figure 3). The 3C.2a
and the 3C.2a1 subclade circulated in approximately equal proportions. A representative
set of 153 influenza A(H3N2) viruses (51 international and 102 United States) were
antigenically characterized, and most (97%) A(H3N2) viruses were well-inhibited (reacting
at titers of less than or equal to fourfold of the homologous virus titer) by ferret
antisera raised against A/Michigan/15/2014 (3C.2a), a cell propagated A/Hong Kong/4801/2014-like
reference virus representing the A(H3N2) component of the 2017 Southern Hemisphere
and 2017–18 Northern Hemisphere influenza vaccines. A smaller proportion (33%) of
influenza A(H3N2) viruses were well-inhibited by antiserum raised against egg-propagated
A/Hong Kong/4801/2014 reference virus representing the A(H3N2) vaccine component,
which is likely because of egg-adaptive amino acid changes in the HA of the egg-propagated
virus.
A total of 85 influenza B/Victoria-lineage viruses were phylogenetically analyzed,
and all HA genes belonged to genetic clade V1A, the same genetic clade as the vaccine
reference virus, B/Brisbane/60/2008. However, two deletion subclades were detected
in 2017. One subclade has a 6-nucleotide deletion (encoding amino acids 162 and 163)
and the other subclade has a 9-nucleotide deletion (encoding amino acids 162, 163
and 164). The 162–163 double deletion in the HA was detected in viruses circulating
in multiple countries, with the majority identified in the United States, although
the three viruses with 162–164 triple deletion were only detected in Hong Kong SAR,
China. Thirty-nine (72%) B/Victoria lineage viruses were well-inhibited by ferret
antisera raised against MDCK-propagated B/Brisbane/60/2008 reference virus, representing
the B/Victoria lineage component of the 2017 Southern Hemisphere and 2017–2018 Northern
Hemisphere influenza vaccines. However, 28% of B/Victoria lineage viruses reacted
poorly with ferret antisera raised against MDCK-propagated B/Brisbane/60/2008, which
correlated with the 162–163 double deletion and the 162–164 triple deletion in the
HA.
Phylogenetic analysis of 180 influenza B/Yamagata-lineage viruses indicate that the
HA genes belonged to clade Y3 (Figure 3). A total of 99 representative influenza B/Yamagata-lineage
viruses (59 international and 40 United States) were antigenically characterized,
and all were antigenically similar to B/Phuket/3073/2013, the reference vaccine virus
representing the influenza B/Yamagata-lineage component of the 2017 Southern Hemisphere
and 2017–18 Northern Hemisphere quadrivalent vaccines.
Composition of the 2018 Southern Hemisphere Influenza Vaccine
The WHO recommendations for influenza vaccine composition for the 2018 Southern Hemisphere
season were made at the WHO Vaccine Consultation meeting September 25–28, 2017, in
Melbourne, Australia. The recommended components for the 2018 Southern Hemisphere
influenza trivalent vaccines are an A/Michigan/45/2015 (H1N1)pdm09-like virus, an
A/Singapore/INFIMH-16-0019/2016 (H3N2)-like virus, and a B/Phuket/3073/2013-like (B/Yamagata
lineage) virus (
8
). For quadrivalent vaccines, an additional component, B/Brisbane/60/2008-like (B/Victoria
lineage) virus, is recommended (
8
). This represents a change in the influenza A(H3N2) component and a change in the
influenza B lineage included in the trivalent vaccine compared with the composition
of the 2017 Southern Hemisphere and 2017–18 Northern Hemisphere influenza vaccine
formulation. The H3N2 component was updated to address the egg-adaptive changes that
occurred with the egg-propagated A/Hong Kong/4801/2014 reference virus and to better
represent genetic changes seen in recently circulating H3N2 viruses.
Antiviral Resistance of Influenza Viruses
The WHO Collaborating Center for Surveillance, Epidemiology, and Control of Influenza
at CDC tested 486 influenza virus specimens collected during May 21–September 23,
2017, from the United States and worldwide for resistance to the influenza neuraminidase
inhibitor antiviral medications currently approved for use against seasonal influenza:
oseltamivir, zanamivir, and peramivir. A total of 75 influenza A(H1N1)pdm09 viruses
(37 international and 38 United States) were tested, and all were sensitive to these
drugs. All 231 influenza A(H3N2) viruses (60 international and 171 United States)
and all 180 influenza B viruses (98 international and 82 United States) tested were
also sensitive to all three recommended antiviral medications. High levels of resistance
to the adamantanes (amantadine and rimantadine) persist among influenza A(H1N1)pdm09
and influenza A(H3N2) viruses. Adamantane drugs continue not to be recommended for
use against influenza at this time.
Discussion
During May 21–September 23, 2017, influenza A(H3N2), influenza A(H1N1)pdm09, and influenza
B viruses co-circulated worldwide. In the United States, influenza B viruses predominated
from late May through late June. Influenza A viruses were most commonly reported beginning
in early July. The majority of the influenza viruses collected from the United States
and other countries during that time were characterized antigenically and genetically
as being similar to the cell-grown reference viruses representing the 2017 Southern
Hemisphere and 2017–18 Northern Hemisphere influenza vaccine viruses. Antigenic and
genetic characterization of circulating influenza viruses can give an indication of
the influenza vaccine's ability to produce an immune response against the wide array
of influenza viruses cocirculating, but vaccine effectiveness studies are needed to
determine how much protection has been provided to the population by vaccination.
Influenza A(H1N1)pdm09 viruses were detected at low levels from May 21 to September
23, and virus characterization data indicate no substantial genetic or antigenic changes,
even among viruses from regions that experienced higher A(H1N1)pdm09 activity. Influenza
A(H3N2) viruses have predominated in many countries in the Southern Hemisphere and
in the United States since early July. Virus characterization data suggest extensive
genetic diversity among circulating viruses, but limited evidence of substantial antigenic
drift. To date, a predominant subclade of A(H3N2) viruses with substantial antigenic
drift has yet to emerge, and extensive genetic variation exists in the circulating
virus population. Among the influenza B viruses for which lineage was determined,
influenza B/Yamagata viruses predominated across the United States from May 21 through
September 23, and virus characterization data indicate no substantial genetic or antigenic
changes. Two subgroups of antigenically distinct influenza B/Victoria viruses, represented
by the double or triple deletion viruses, were detected; the majority of the double
deletion viruses were identified in the United States, while all three triple deletion
viruses were identified only in Hong Kong SAR, China. Nevertheless, such antigenically
distinct viruses represented a minority of B/Victoria viruses circulating globally
during this period. Close monitoring of these viruses is required to better assess
their potential impact on public health. Although influenza B viruses circulate throughout
the influenza season, they frequently circulate later in the season than do influenza
A viruses and often result in a second peak of influenza activity, often in the late
winter and spring in the United States and other Northern Hemisphere countries (
3
).
Annual influenza vaccination is the best method for preventing influenza and its potentially
severe complications (
9
). In the United States, annual influenza vaccination is recommended for all persons
aged ≥6 months who do not have contraindications. Annual influenza vaccination is
recommended regardless of whether the vaccine composition has changed because immunity
from vaccination wanes over time and might decline below protective levels after one
season. Optimally, vaccination should occur before the onset of influenza activity
in the community. If possible, vaccination should be offered by the end of October
and should continue to be offered as long as influenza viruses are circulating and
unexpired vaccine is available. Children aged 6 months through 8 years who require
2 doses should receive their first dose as soon as possible after vaccine becomes
available, and the second dose ≥4 weeks later. For 2017-18 season, manufacturers have
projected they will supply the United States with as many as 151 to 166 million doses
of injectable influenza vaccine; approximately 119 million of this will be quadrivalent
vaccine. As of September 15, 2017, approximately 73 million doses had already been
distributed.
Multiple influenza vaccines are approved and recommended for use and are being distributed
during the 2017–18 season, including egg-based trivalent and quadrivalent inactivated
influenza vaccines (IIV3 and IIV4), adjuvanted trivalent egg-based inactivated influenza
vaccines (aIIV3), high-dose trivalent egg-based inactivated influenza vaccines (HD-IIV3),
quadrivalent cell culture–based inactivated influenza vaccines (ccIIV4), and recombinant
trivalent and quadrivalent influenza vaccines (RIV3 and RIV4). Two available intramuscular
vaccines are approved for administration by jet injector for persons aged 18 through
64 years. One IIV4 formulation is approved for intradermal administration. There is
no preferential recommendation for one licensed and recommended influenza vaccine
product over another for persons for whom more than one licensed, recommended product
is available (
9
). Currently available influenza vaccines, with the exceptions of RIV3, RIV4, and
ccIIV4, are prepared by propagation of virus in embryonated eggs (
9
). Egg propagation of influenza A(H3N2) viruses often leads to genetic changes that
have antigenic implications. For the 2017–18 season inactivated vaccines, all influenza
A(H1N1) and A(H3N2) and both influenza B components will be egg-derived, with the
exception of ccIIV4, for which the influenza A(H3N2) virus component will, for the
first time, be a cell-derived vaccine virus component (
9
). This represents a first step toward producing a totally egg-independent inactivated
virus vaccine. Recombinant technology is used in the production of RIV3 and RIV4;
therefore they are manufactured without the use of influenza viruses or eggs. The
use of egg-independent vaccine technologies is likely to provide vaccines that more
precisely represent the antigenic characteristics of circulating viruses and have
the potential to offer improved protection. Because of the low effectiveness of live
attenuated intranasal influenza vaccine (LAIV4) against influenza A(H1N1)pdm09 viruses
in the United States during the 2013–14 and 2015–16 seasons, for the 2017–18 season,
the Advisory Committee on Immunization Practices and CDC renewed the recommendation
that LAIV4 should not be used (
9
).
Although vaccination is the best method for preventing and reducing the impact of
influenza, antiviral medications provide a valuable adjunct. Treatment with influenza
antiviral medications as early as possible in the course of illness is recommended
for patients with confirmed or suspected influenza (either seasonal influenza or novel
influenza virus infection) who have severe, complicated, or progressive illness; who
require hospitalization; or who are at high risk for influenza-related complications
¶¶¶¶
(
10
). Treatment is most effective when given early in the illness, especially within
48 hours of illness onset; providers should not delay treatment until test results
become available and should not rely on insensitive assays such as found with some
rapid antigen detection influenza diagnostic tests to determine treatment decisions
(
10
).
Fifty-one infections with variant influenza viruses were reported from five states
during summer 2017. Most of these infections occurred in children with prior direct
contact with pigs at agricultural fairs, highlighting the importance of preventive
actions,***** especially for young children or persons at high risk for serious influenza
complications. Although community transmission of these viruses has not been identified,
the potential for them to develop the ability to transmit efficiently from person
to person remains a concern. Testing for seasonal influenza viruses and monitoring
for novel influenza A virus infections should continue year-round. Health care providers
also are reminded to consider novel influenza virus infections in persons with influenza-like
illness and swine or poultry exposure, or with severe acute respiratory infection
after travel to areas where avian influenza viruses have been detected. Providers
should alert the local public health department if novel influenza virus infection
is suspected. Clinical laboratories using a commercially available influenza diagnostic
assay that includes influenza A virus subtype determination should contact their state
public health laboratory to facilitate transport and additional testing of any specimen
that is positive for influenza A, but for which the subtype cannot be determined.
Public health laboratories should immediately send influenza A virus specimens that
they cannot subtype using standard methods to CDC and submit all specimens that are
otherwise unusual as soon as possible after identification. Early identification and
investigation of human infections with novel influenza A viruses are critical to ensure
timely risk assessment so that appropriate public health measures can be taken.
Influenza surveillance reports for the United States are posted online weekly (https://www.cdc.gov/flu/weekly).
Additional information regarding influenza viruses, influenza surveillance, influenza
vaccine, influenza antiviral medications, and novel influenza A infections in humans
is available at https://www.cdc.gov/flu.
Summary
What is already known about this topic?
CDC collects, compiles, and analyzes data on influenza activity year-round in the
United States. Timing of influenza activity and predominant circulating influenza
viruses vary by season.
What is added by this report?
Worldwide, influenza activity during May 21–September 23, 2017, followed typical seasonality
and in the United States overall, low levels of seasonal influenza activity were detected.
The majority of influenza viruses genetically and antigenically characterized at CDC
were similar to the reference viruses representing the recommended components for
the 2017–18 vaccine. A small subset of antigenically distinct influenza B/Victoria
viruses was detected.
What are the implications for public health practice?
In the United States, an annual influenza vaccination is recommended for all persons
aged ≥6 months and can reduce the likelihood of becoming ill with influenza and transmitting
the virus to others. Annual influenza vaccination offers optimal protection regardless
of whether the vaccine composition has changed since the previous season, because
immunity wanes over time. Although vaccination is the best method for preventing and
reducing the impact of influenza, antiviral medications are an important adjunct.
Early treatment with influenza antiviral medications is recommended for patients with
confirmed or suspected influenza (either seasonal influenza or novel influenza virus
infection) who have severe, complicated, or progressive illness; who require hospitalization;
or who are at high risk for influenza-related complications. Testing for seasonal
influenza viruses and monitoring for novel influenza A virus infections should continue
year-round.