<h2>Classical FD (&lt;3% enzyme activity)</h2>

Neuropathic pain, angiokeratomas, and/or cornea verticillata are absent in females.

Childhood and adolescence

<table border="0" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td>
 <h3>Nonclassical or late-onset FD (3%–30% enzyme activity)</h3></td>
 </tr>
 <tr>
 <td>Variable disease course and single organ involvement</td>
 </tr>
 <tr>
 <td>Cardiac variant is common in late-onset FD</td>
 </tr>
 <tr>
 <td>Identified in patients with stroke, renal failure, or cardiomyopathy</td>
 </tr>
 <tr>
 <td>No neuropathic pain, angiokeratomas, and/or cornea verticillata</td>
 </tr>
 </tbody>
</table>

black

FD diagnosis requires a multidisciplinary team approach involving:

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center;">Biochemist</td>
 </tr>
 </tbody>
</table>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center;">Pediatrician</td>
 </tr>
 </tbody>
</table>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center;">Neurologist</td>
 </tr>
 </tbody>
</table>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center;">Cardiologist</td>
 </tr>
 </tbody>
</table>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center;">Dermatologist</td>
 </tr>
 </tbody>
</table>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center;">Nephrologist</td>
 </tr>
 </tbody>
</table>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center;">Geneticist</td>
 </tr>
 </tbody>
</table>

Suggested diagnostic algorithm for patient with clinically suspected FD

<h3>1.&nbsp;Lyso-Gb3 indicates severity of FD</h3>
2.&nbsp;Endomyocardial and renal biopsies are used
3.&nbsp;Genetic testing

<h3>Testing for FD</h3>

<ul>
 <li>Causative mutation</li>
 <li>Affected family members</li>
 <li>Eligibility for treatment with migalastat</li>
</ul>

LSD referral centers to manage FD from diagnosis to long-term follow-up

<table border="0" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td>
 Rare but underdiagnosed</td>
 <td>
 To be known and recognized by internal medicine physicians</td>
 <td>
 Early treatment can change the natural course of the disease.</td>
 </tr>
 </tbody>
</table>

FD:

*Eye involvement includes cornea verticillata, tortuous retinal vessels, cataracts, and conjunctival lymphangiectasia. 
 Rare but To be known and recognized by underdiagnosed internal medicine physicians α-Gal A: Alpha-galactosidase; eGFR: Estimated glomerular filtration rate; GLA: α-Galactosidase A; FD: Fabry disease; GI: Gastrointestinal; LSD: Lysosomal storage disease; Lyso-Gb3: Globotriaosylsphingosine; TIA: Transient ischemic attack.

Reference

DIAGNOSING FABRY DISEASE IN CLINICAL PRACTICE

FABRY

RARE-DISEASE

<h2>RSV Is Seasonal, With Peak Incidence Varying by Region1,2</h2>

<ul>
 <li>Temperate countries in the&nbsp;Northern Hemisphere&nbsp;generally experience the start of the RSV season between September and January.</li>
 <li>Those in the&nbsp;Southern Hemisphere&nbsp;generally experience the start of the RSV season between March and June, closely aligned with colder temperatures.</li>
 <li>The seasonality of RSV in&nbsp;(sub)tropical climates&nbsp;appears less consistent—with studies indicating peak of RSV season closely aligns with the rainy season and/or higher temperatures.</li>
</ul>

<h2>RSV is a highly transmissible viral disease</h2>

<ul>
 <li>RSV&nbsp;is transmitted by respiratory droplets and considered “highly contagious”9-11</li>
 <li>R0&nbsp;of&nbsp;&nbsp;4.5 
 mean R0&nbsp;ranging from 1.7 to 8.212</li>
</ul>

References

<h2>RSV shedding in Infants, toddlers and immunecompromised</h2>

Duration of Virus Shedding in Infants and Toddlers

Duration of Virus Shedding in Immunecompromised patients

<h2>Most Infants Are Exposed to RSV Infection in the Community and Through Other Children1-3</h2>

Crowding and day-care exposure significantly increased the risk of severe RSV disease4-6

In the United States,&nbsp;more than 50 per cent of under-ones&nbsp;are in some form of childcare;&nbsp;~75% from the age of 4 months7
Network showing the sources of infection to the infant, as identified by social relationships in Kenya.1 The size of the circles is proportional to the number of cases.

RESPIRATORY-SYNCYTIAL-VIRUS

VACCINES

All Infant Protection

RSV is a leading cause of hospitalization in all infants

All infants need protection from RSV

<h2>Most Hospitalizations for RSV occur in Healthy Full Term Infants1-3</h2>

<a href="https://publications.aap.org/pediatrics/article-abstract/132/2/e341/31332/Respiratory-Syncytial-Virus-Associated?redirectedFrom=fulltext?autologincheck=redirected">Respiratory Syncytial Virus–Associated Hospitalizations Among Children Less Than 24 Months of Age | Pediatrics | American Academy of Pediatrics (aap.org)</a>
aEstimate includes previously healthy premature subjects &lt;37 weeks’ gestation, and less than 2 years old.

<h2>RSV Infant ICU Admissions and Mechanical Ventilation in the US1</h2>
Surveillance through the Influenza Hospitalization Surveillance Network from October 2014-April 2015

Infant RSV ICU Admissions&nbsp;(n=336) 
 &nbsp;
<ul>
 <li>26%&nbsp;(221/851) of hospitalized&nbsp;healthy term infants&nbsp;were admitted to&nbsp;ICU1</li>
</ul>

Infant RSV Requiring Mechanical Ventilation&nbsp;(n=82)
<ul>
 <li>22% (49/221)&nbsp;of ICU admitted&nbsp;healthy term infants&nbsp;required&nbsp;mechanical ventilation1</li>
</ul>

CMC: chronic medical condition (includes chronic lung disease, cardiovascular disease, upper airway abnormality, asthma, neurologic/neuromuscular conditions, blood disease, renal disorder, immunocompromised, chronic metabolic disease, liver disease, and other);&nbsp;ICU: Intensive Care Unit; Preterm: born at &lt;37 weeks gestational age; Term: born at 37+ weeks gestational age. Data from the US, % of Infant RSV ICU admissions may vary in other countries.
<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7107566/">Estimated Burden of Community-Onset Respiratory Syncytial Virus–Associated Hospitalizations Among Children Aged &lt;2 Years in the United States, 2014–15 - PMC (nih.gov)</a>

<h3>"There is an urgent and universal need to develop products to reduce child mortality and morbidity through prevention of RSV disease"+</h3>
Ruth A. Karron, 
 MD Center for Immunization Research Department of International Health Johns Hopkins Bloomberg School of Public Health Baltimore, MD, USA Science. May 14, 2021:Vol. 372, Issue 6543, pp 686-687.

<h3>"Because most children hospitalized with RSV have no underlying medical condition or history of prematurity, interventions against RSV used to broadly target all young infants are likely to result in the greatest impact. "</h3>
Brian Rha, MD MSPH 
 Division of Viral Diseases Centers for Disease Control and Prevention Atlanta, GA, USA Pediatrics. July 2020: Vol. 146, Issue 1, p. e20193611.

<h3 style="text-align: center;">Methods</h3>

Compare passive immunization with LA mAb for all infants to the current standard of care using a static decision-analytic model in a cohort of KSA infants experiencing their first RSV season 
 &nbsp;
Subpopulations: 
 &nbsp;
<ul>
 <li>term and late preterm infants (≥35 wGA)</li>
 <li>Healthy preterm infants (29w GA - 34w6d GA, not eligible for palivizumab)</li>
 <li>palivizumab-eligible infants* 
 According to the SIBRO guidelines</li>
</ul>

STUDY DESIGN

Entire KSA infant birth cohort(&lt;12 months of age) during their 1st RSV season 
 (October – March)

PARTICIPANTS &amp; SEASON

Standard of Care:&nbsp;healthy infants born at least 29w GA, administered monthly to eligible infants during the season LA mAb (Nirsevimab) Single dose administered to all infants at the beginning of the RSV season or at birth

IMMUNIZATION STRATEGIES

Static decision-analytic model 
 RSV burden and nirsevimab impact were considered and stratified by: 
 &nbsp;
<ul>
 <li>Population-based approach (comorbidities, monoclonal antibody)</li>
 <li>Age-based approach</li>
</ul>

ANALYSIS

<h3 style="text-align: center;">Assumptions</h3>
Hospitalizations rates per age groups &amp; subpopulations in local birth cohort in KSA
2021 Saudi birth = 509,139

<h4>Highest risk of hospitalizations</h4>
Per subpopulation
<ul>
 <li>Palivizumab eligible: early preterm ≤28 weeks of GA, with CHD or CLDP</li>
 <li>Preterm infants &gt;28 weeks of GA</li>
</ul>
Per chronological age
<ul>
 <li>with risk decreasing with increasing age in months</li>
</ul>

CHD,&nbsp;congenital heart disease;&nbsp;CLDP,&nbsp;chronic lung disease of prematurity;&nbsp;GA,&nbsp;gestational age; mo, month. 
 Ahmed A, Parveen S, Al-Hassinah SM, Al-Amery SF. An overview of respiratory syncytial virus infections in Saudi Arabia. The Journal of Infection in Developing Countries. 2018;12(11):929-36

<h3 style="text-align: center;">Results</h3>
Disease burden under the current standard of care

<h3 style="text-align: center;">428,264 RSV cases 
 84%&nbsp;from KSA birth cohort</h3>
Distribution of RSV MALRTIs by health event over the first RSV season of KSA infants 
 &nbsp;

<h3 style="text-align: center;">SAR ~607 million</h3>
Direct economic burden of RSV in infants
Distribution of RSV MALRTIs by related direct medical costs over the first RSV season of KSA infants

Percentages may not add to 100% due to rounding. All costs are in 2021 United States dollars. ED,&nbsp;emergency department;&nbsp;ICU,&nbsp;intensive care unit;&nbsp;MV,&nbsp;mechanical ventilation;&nbsp;LRTI,&nbsp;lower respiratory tract illness;&nbsp;MA,&nbsp;medically attended;&nbsp;RSV,&nbsp;respiratory syncytial virus;&nbsp;SoC,&nbsp;standard of care;&nbsp;US,&nbsp;United States.

<h2>Red Flags</h2>
<ul>
 <li>
 84 % from KSA birth cohort infected annually by RSV</li>
 <li>
 Among those hospitalized, 18% were admitted to a PICU , and 2% required MV</li>
 <li>
 RSV hospitalized cases accounted for &lt;6% of overall RSV-LRTIs burden, the associated with 60% direct cost.</li>
 <li>
 607 million Annually direct cost of RSV burden in Saudi Arabia</li>
 <li>
 Indirect effects were not captured, so potential benefits on indirect costs and virus spread were not estimated</li>
</ul>

<h3 style="text-align: center;">Results</h3>
Impact of LA mAb for all KSA infants
Cases Vs budget saving

<h3>Reduce RSV cases by more than 50% and associated healthcare costs by more than 60%</h3>
*Includes hospitalization that resulted in ICU admission or MV.
ED,&nbsp;emergency department;&nbsp;ICU,&nbsp;intensive care unit;&nbsp;MV,&nbsp;mechanical ventilation;&nbsp;RSV,&nbsp;respiratory syncytial virus;&nbsp;US,&nbsp;United States.

RSV Burden in Infants

<h2>Study Objective</h2>
<h3>Guideline development process: AGREE II system and classification</h3>
<ul>
 <li>To develop clinical guidelines</li>
 <li>Standard of care for ASMD patients</li>
 <li>Using an SLR and the experiences of multidisciplinary experts (GDG)</li>
</ul>

<h2>Experts’ Recommendations for Classification and Diagnosis of ASMD</h2>

Acute neurovisceral, ASMD type A 
 Hepatosplenomegaly, proatherogenic lipid profile, thrombocytopenia, interstitial lung disease, skeletal involvement, liver disease, cherry red macula, hypotonia, and&nbsp;rapidly progressive neurodegeneration
Chronic neurovisceral, ASMD type A/B 
 All symptoms of ASMD type A along with&nbsp;delayed growth and puberty, slowly progressive neurodegeneration and cherry red macula (in few patients), and hypotonia
Chronic visceral, ASMD type B 
 All symptoms of type A/B&nbsp;with the absence of hypotonia and neurodegeneration and few patients with cherry red macula

<h2>Experts’ Recommendations for the Management of ASMD</h2>

<h3>Multidisciplinary assessment&nbsp;is recommended for all ASMD patients or as needed by:</h3>
<ul>
 <li>Primary care physician</li>
 <li>Metabolic diseases specialist</li>
 <li>Neurologist</li>
</ul>

<h3>Management of ASMD</h3>
ERT
<ul>
 <li>All patients with a confirmed diagnosis of ASMD and significant non-CNS</li>
 <li>Effectiveness of treatment should be monitored</li>
</ul>
Use of HSCT is experimental
<h3>Symptomatic treatment</h3>
<ul>
 <li>CLD should be monitored and treated for gastrointestinal bleeding</li>
 <li>Pulmonary disease may require long-term oxygen therapy</li>
</ul>

<h3>Recommended assessments for all ASMD patients</h3>
<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td>Assesment</td>
 <td>Frequency</td>
 </tr>
 <tr>
 <td>Baseline history</td>
 <td>At diagnosis 
 <ul>
 <li>Assess recurrent chest infections at diagnosis, then at each visit</li>
 </ul></td>
 </tr>
 <tr>
 <td>Pulmonary assessment</td>
 <td>
 <ul>
 <li>Chest radiograph and/or high-resolution chest CT to assess the extent of interstitial lung disease at diagnosis regardless of age, then every 2–4 years</li>
 </ul></td>
 </tr>
 <tr>
 <td>Musculoskeletal assessment</td>
 <td>At diagnosis, then at each visit</td>
 </tr>
 <tr>
 <td>Ophthalmologic evaluation</td>
 <td>At diagnosis</td>
 </tr>
 </tbody>
</table>

Abbreviations

Consensus Guidelines for the Clinical Management of ASMD

ACID-SPHINGOMYLENASE-DEFICIENCY-NIEMANN-PICK

<h2>Study objective and method</h2>
To demonstrate

The benefits of adding lyso-GL-3&nbsp;to&nbsp;►

Primary diagnostic for testing&nbsp;for&nbsp;►

Improving detection rate of potential females with FD

Avoiding unnecessary genetic testing

<table align="center" border="1" cellpadding="1" cellspacing="1" style="width: 1120px;">
 <tbody>
 <tr>
 <td>
 First large prospective study</td>
 </tr>
 </tbody>
</table>

11,948&nbsp;females with suspicion of FD
&nbsp;
tested for

Biochemical tests
<ul>
 <li>α-Gal A activity</li>
 <li>Lyso-GL-3 levels</li>
</ul>
&nbsp;
followed by

Genetic confirmatory testing in&nbsp;883&nbsp;females

<table align="center" border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td rowspan="7">
 <h3 style="text-align: center;">Groups</h3></td>
 <td style="text-align: center; vertical-align: top;">01.&nbsp;Low α-Gal A activity High lyso-GL-3</td>
 <td style="text-align: center; vertical-align: top;">02.&nbsp;Low α-Gal A activity Normal lyso-GL-3</td>
 <td style="text-align: center; vertical-align: top;">03.&nbsp;Normal α-Gal A activity High lyso-GL-3</td>
 <td style="text-align: center; vertical-align: top;">04.&nbsp;Normal α-Gal A activity Normal lyso-GL-3</td>
 </tr>
 <tr>
 <td colspan="1" style="text-align: center; vertical-align: top;">Classical FD very likely (n=61)</td>
 <td style="text-align: center; vertical-align: top;">Classical FD unlikely (n=184)</td>
 <td style="text-align: center; vertical-align: top;">
 FD very likely (n=256)</td>
 <td style="vertical-align: top;">
 95.8 had normal results (n=11,447*)</td>
 </tr>
 <tr>
 <td colspan="3" rowspan="1" style="text-align: center;">Genetic confirmatory test</td>
 <td style="text-align: center;">No further testing required</td>
 </tr>
 </tbody>
</table>

(184/883) females were identified with one or two&nbsp;GLA&nbsp;variants.

<table align="center" border="1" cellpadding="1" cellspacing="1" style="width:500px;">
 <tbody>
 <tr>
 <td style="text-align: center;">Distribution of genetically positive samples</td>
 </tr>
 </tbody>
</table>

Better indicator of FD

Elevated lyso-GL-3 levels (39% PPV)

Clearly negative results for both biochemical parameters:
Unlikely to have FD, even in clinically highly suspicious cases

<table align="center" border="1" cellpadding="1" cellspacing="1" style="width: 1120px;">
 <tbody>
 <tr>
 <td style="text-align: center;">Proposed diagnosis decision tree</td>
 </tr>
 </tbody>
</table>

<h3>STEP 2</h3>
Once enzyme deficiency is confirmed, molecular testing is performed to identify GLA genetic variants.

<h3>STEP 2</h3>
Once enzyme activity (deficient or not) together with elevated biomarker is confirmed, molecular testing is performed to identify GLA genetic variants.

*Mutation analysis performed in 389 cases.
α-Gal A: Alpha-galactosidase A; dbFGP: Fabry disease genotype–phenotype database; FD: Fabry disease; Lyso-GL-3: Globotriaosylsphingosine; PPV: Positive predictive value; DBS: Dried blood spotting; GLA: Galactosidase alpha; VUS: Variant of unknown significance.

BIOCHEMICAL DIAGNOSTIC STRATEGY IN FEMALES SUSPECTED OF FABRY DISEASE

<h2>What molecular pathways are implicated in cGVHD?</h2>
Several pathways have been shown to be key mediators of disease progression in chronic graft-versus-host disease.1

The rho-associated coiled-coil–containing protein kinase (ROCK) molecular pathway plays a key role in immune and fibrotic disease.2,3&nbsp;Additionally, ROCK is downstream of major profibrotic mediators and regulates multiple fibrotic processes, such as myofibroblast activation and profibrotic gene transcription.3 ROCK2, specifically, is involved in both the inflammatory and fibrotic components of cGVHD and has been shown to play an important role in modulating immune homeostasis.2 
 Selective ROCK2 inhibition has been shown to help resolve immune dysregulation by downregulating pro-inflammatory T helper (Th) 17 cells and increasing regulatory T (Treg) cells.2&nbsp;Furthermore, selective ROCK2 inhibition has been shown to downregulate key fibrotic processes, such as TGF-β and LPA, leading to a decrease in fibrosis and collagen deposition.3-5

ROCK

Following HCT, B-cell homeostasis and tolerance mechanisms are disrupted, resulting in reduced memory B-cell formation.6&nbsp;These host-reactive B cells are associated with the development of cGVHD.7 
 BTK is a signaling molecule of the B-cell antigen receptor and cytokine receptor pathways,8&nbsp;which is expressed mainly in B cells and other hematopoietic tissues.9&nbsp;Signaling via BTK results in the activation of pathways necessary for B-cell trafficking, chemotaxis and adhesion.8

JAK1 and JAK2 are signal mediators of several cytokines and growth factors that are necessary for hematopoiesis and immune function. STATs are recruited to cytokine receptors during JAK signaling, leading to modulation of gene expression.10 In cGVHD pathogenesis, JAK-STAT molecular pathways regulate the development, proliferation and activation of various immune cell types.10

IL-2, a cytokine signaling molecule, is essential for normal Treg cell development, expansion, activity and survival. CD4+&nbsp;Treg cells play a role in immune tolerance and controlling immune responses.&nbsp;Impaired Treg cell function is characteristic of cGVHD and is associated with loss of tolerance and autoimmunity.11

IL-2

Research continues to uncover the role of these pathways.

Learn more about inflammation and fibrosis

What manifestations are caused by the activation of these pathways?

Molecular Pathway

CHRONIC-GRAFT-VERSUS-HOST-DISEASE-CGVHD

TRANSPLANT

<div>
 <h2>GENETIC PROFILE</h2>
 ASMD is an autosomal recessive LSD caused by pathogenic variants in the ASM enzyme–encoding gene sphingomyelin phosphodiesterase 1 (SMPD1). 
 Sphingomyelin helps regulate cellular processes, such as cell cycle regulation, cell signaling, and apoptosis. 
 When ASM activity is deficient, sphingomyelin cannot be sufficiently metabolized; it accumulates in lysosomes, particularly in macrophages and hepatocytes. This accumulation damages cells in multiple organs, leading to potentially life-threatening complications. 
 Males and females have an equal chance of being affected4
</div>

Historically known as Niemann-Pick disease type A (NPA) or infantile neurovisceral ASMD
<ul>
 <li>Onset: Early Infancy</li>
 <li>Phenotype: Rapidly progressive with acute multiorgan manifestations and neurodegeneration</li>
 <li>Life Expectancy: 2 to 3 years of age</li>
</ul>

Type A

Historically known as Niemann- Pick disease type A/B (NPA/B) or chronic neurovisceral ASMD
<ul>
 <li>Onset: Infancy to childhood</li>
 <li>Phenotype: Variably progressive with multiorgan manifestations and differing degrees of neurologic involvement</li>
 <li>Life Expectancy: Between early childhood and adulthood</li>
</ul>

Type A/B

Historically known as Niemann- Pick disease type B (NPB) or chronic visceral ASMD
<ul>
 <li>Onset: Infancy to childhood</li>
 <li>Phenotype: Chronic with multiorgan manifestations and no or only minor neurologic involvement</li>
 <li>Life Expectancy: Between childhood and late adulthood</li>
</ul>

Type B

The rarity of ASMD, heterogeneity of its manifestations, and challenging differential diagnosis can result in delayed diagnosis and management of patients.
Early diagnosis of ASMD is critical for appropriate management.

<h3>IMPORTANCE OF EARLY DIAGNOSIS</h3>

A simple enzyme activity test can be performed on a DBS (dried blood spot) to indicate reduced ASM activity.
A positive DBS enzyme assay is highly indicative of ASMD, but an analysis from a whole blood sample and/or genetic testing is required to confirm the diagnosis.5

HOW TO DIAGNOSE

Identifying known disease-causing alleles of ASMD allows for
<ol>
 <li>Individual genetic counseling</li>
 <li>Carrier screening for at-risk individuals</li>
 <li>Family planning</li>
</ol>

ASMD

<h3>Avoiding influenza may reduce the risk of influenza-related heart attack3:</h3>
META-ANALYSIS: Estimates of interventional efficacy in secondary prevention of myocardial infarction3

<h3>Avoiding influenza can help reduce the risk of severe outcomes4:</h3>
In 124,503 people with type 2 diabetes, from 2003-2010, influenza vaccination was associated with substantial reductions in hospital admission rates.4

aNot significant. 
 AMI=acute myocardial infarction.

<h3>The CDC Advisory Committee on Immunization Practices (ACIP) recommends routine annual influenza vaccination for all eligible persons aged ≥6 months5:</h3>
While the ACIP recommends all persons aged 6 months and older who do not have contraindications receive an influenza vaccine, it is especially important for populations who are at increased risk for severe illness and medical complications. These include, but are not limited to, adults aged 50 years and older and people who have5:
<ul>
 <li>Chronic pulmonary disorders (including asthma)</li>
 <li>Cardiovascular diseases (excluding isolated hypertension)</li>
 <li>Metabolic disorders (including diabetes)</li>
</ul>
<h3>The ACIP recommends being vaccinated against influenza by the end of October each year5:</h3>
Since the timing of the influenza season is unpredictable and vaccine-induced immunity may wane over time, the ACIP suggests the following timing recommendations5:
DON’T VACCINATE TOO EARLY: Early vaccination in July or August for nonpregnant adults should be avoided because it may be associated with decreased vaccine effectiveness before the end of the influenza season, especially for older adults.5
OFFER VACCINATIONS THROUGH FLU SEASON: Vaccination should continue to be offered as long as influenza viruses are circulating.5

Flu and Vaccination

INFLUENZA

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