Franzeska Anna

INFLUENZA VIRUS
INFLUENZA VIRUS TYPES
INFLUENZA A VIRUS

 Ini adalah gambar virus

influenza (flu) A.
 Virus influenza A
diklasifikasikan berdasarkan
subtipe berdasarkan sifat
protein permukaan
hemagglutinin (H atau HA)
dan neuraminidase (N atau
NA).
 Ada 18 subtipe HA yang
berbeda dan 11 subtipe NA
yang berbeda.
 Subtipe diberi nama dengan
menggabungkan angka H dan
N – misalnya, A(H1N1),
A(H3N2).
 Virus influenza A dibagi menjadi subtipe berdasarkan dua protein pada
permukaan virus: hemagglutinin (H) dan neuraminidase (N).
 Ada 18 subtipe hemaglutinin yang berbeda dan 11 subtipe neuraminidase yang
berbeda (masing-masing H1 hingga H18 dan N1 hingga N11). Ada potensi lebih
banyak lagi kombinasi subtipe influenza A mengingat kecenderungan untuk
“reassortment” virus. Reassortment dapat terjadi ketika dua virus influenza
menginfeksi inang pada saat yang sama dan bertukar informasi genetik.
 Subtipe influenza A dapat dipecah lebih lanjut menjadi “clade” dan “sub-
clade” genetik yang berbeda. Lihat grafik “Virus Influenza” di bawah ini
untuk gambaran visual dari klasifikasi ini.
INFLUENZA VIRUS
PATHOGENESIS
PEOPLE AT INCREASED RISK OF COMPLICATIONS
 The co-pathogenesis of influenza viruses
with bacteria in the lung

• Several virulence factors that are expressed by influenza viruses can directly
interact with the lungs or with the host immune system.
• Haemagglutinin mediates attachment by binding to terminal sialic acids on cell
surface proteins and initiating endocytosis. A variety of extracellular proteins
can bind to glycans on haemagglutinin and neutralize or help to eliminate
viruses from the lower
respiratory tract.
• Viruses with a poorly glycosylated haemagglutinin and the ability to engage
both α2,3- and α2,6-linked sialic acids as receptors are able to penetrate deep
into the lungs. The sialidase activity of the neuraminidase protein cleaves sialic
acids from the surface of epithelial cells and from mucins that try to bind and
eliminate virions — this facilitates bacterial access to receptors. The
non-structural proteins PB1-F2 and NS1 are made in infected cells. PB1-F2
causes cytotoxicity and promotes inflammatory responses to co-pathogens; NS1
modulates innate pathways, including interferon signalling

McCullers JA. The co-pathogenesis of influenza viruses with bacteria in the lung. Nature Reviews. Microbiology. 252-62 (2014)
The co-pathogenesis of influenza viruses
with bacteria in the lung

• These virus-mediated effects engender changes in the

physical properties of the lungs and compromise innate
immunity at several levels.
• Epithelial damage and increased receptor availability
enable bacteria to adhere and grow. Depletion of the
specific subset of lung macrophages that is functionally
capable of phagocytosing bacteria enables escape from
early innate immunity.
• Anergy of the primary bacterial sensing apparatus of the
immune system, pattern recognition receptors, such as the
Toll-like receptors (TLRs), prolongs this window of
susceptibility for weeks, while a dysfunctional and
paradoxically over-exuberant inflammatory response that
is characterized by neutrophil
influx and cytokine storm furthers the acute lung injury
that has been started by the virus

McCullers JA. The co-pathogenesis of influenza viruses with bacteria in the lung. Nature Reviews. Microbiology. 252-62 (2014)
The co-pathogenesis of influenza viruses
with bacteria in the lung

• Bacteria that express specific virulence factors may take advantage

of these changes to the host, grow unchecked and cause disease.
• Adherence factors, such as pneumococcal surface protein A or
staphylococcal MSCRAMMs (microbial surface components
recognizing adhesive matrix molecules), enable bacteria to attach to
newly uncovered receptors or to the matrix of collagen and fibrin
that has been laid down as a scaffold for repair.
• Bacterial cytotoxins synergize with their viral counterparts to further
the physical and immune-mediated damage to the lungs. Specific
characteristics of some bacterial strains, such as a thick,
complement-resistant capsule, and a set of unknown proteins
whose existence can be inferred but have not yet been described,
enable improved survival, growth and pathology in virus-infected
hosts.

McCullers JA. The co-pathogenesis of influenza viruses with bacteria in the lung. Nature Reviews. Microbiology. 252-62 (2014)
The co-pathogenesis of influenza viruses with bacteria in the lung

McCullers JA. The co-pathogenesis of influenza viruses with bacteria in the lung. Nature Reviews. Microbiology. 252-62 (2014)
• A schematic model of the pathogenesis of influenza-
induced ARDS. In a healthy lung, the alveolar lumen is
free of fluid to ensure optimum gas exchange (upper
right quadrant).
• After infection, influenza A virus induces epithelial cell
death,
resulting in leakage of proteinaceous fluid into the
alveolar lumen (lower right quadrant).
• Influenza virus also induces cytokine production by
epithelial and endothelial cells, and selectin
upregulation on endothelial cells. Selectin upregulation
on endothelial cells enables extravasation of
neutrophils, which are among the first cells recruited to
the lung in influenza virus infection (lower left
quadrant).
• Neutrophils damage the epithelial–endothelial barrier
via the release of toxic granules and cytokine
production, resulting in increased leakage of
proteinaceous fluid into the alveolar lumen. Selectin
upregulation on endothelial cells enables extravasation
of macrophages, which damage the barrier via the
production of NO, TRAIL, and cytokines (upper left
quadrant).
• In addition to proteinaceous fluid and infiltrating
leucocytes, the progressive damage to the epithelial–
endothelial barrier results in fibrin deposition and
haemorrhage into the alveolar lumen

Short KR, Veldhuis Kroeze EJB, Fouchier RAM. Pathogenesis of

influenza-induced acute respiratory distress syndrome. Lancet. 2013.
 TREATMENT OF INFLUENZA
Most people with influenza who are otherwise healthy do not need special drugs or treatment.
• Rest
• Drinks lots of fluids
• Eat a light diet
• Stay at home
• Take appropriate medicines
• Antiviral drugs
• Antiviral treatment last for 3-5 days and must be started with in the first 2 days of illness
RECOMMENDATIONS FOR
PRACTICE
ANTIVIRUS DRUGS
VAKSINASI INFLUENZA

Kapan Waktu yang Tepat Memberikan Vaksin Influenza?

 Pemberian imunisasi untuk mencegah influenza bisa dilakukan mulai usia 6 bulan.
Pada orang dewasa, WHO merekomendasikan pemberian vaksin satu kali setiap
tahun.
 Di Indonesia, terdapat Vaksin Influenza Trivalent ( Flubio) dan Ada Quadrivalent
(Vaxigrip tetra).
 Di negara beriklim tropis seperti Indonesia, wabah flu bisa terjadi kapan pun. Oleh
karena itu, tidak ada waktu tertentu untuk mendapatkan vaksin influenza.

Berapa Kali Vaksin Influenza Diberikan?

 Pada orang dewasa, PAPDI merekomendasikan pemberian vaksin influenza satu kali
setiap tahun.