Oleh :

Dr. dr. Hj. Efrida Warganegara, M.Kes., Sp.MK

 Classification
• Family Orthomyxoviridae
Myxo = mucus  ability virus to attach to
mucoprotein cell surface; ortho = true
=regular = orthodox
• There are 3 species  1). A; 2). B; and
3). C  not infected human
• Morfologi : virion 100-200 nm in diameter,
symetry is helical, 500 projecting spikes
(80% are HA)
• There are 8 discrete fragment of RNA
genome, HA and NA protein are coded by
segment 4 and 6
Virus – 3. Influenza
 Struktur Virus
 Hemagglutinin (HA) : merupakan glikoprotein bentuk
batang dengan penampang berbentuk segitiga. Antigen ini
mempunyai peranan penting dalam perlekatan dan
masukknya virus ke sel host dan dalam penentuan
virulensi.
 Neuraminidase (NA) : dapat merusak reseptor neuraminic
/ sialic acid pada sel host sehingga berperan dalam
penempelan virus. Tetapi, fungsi yang utama adalah dalam
pembebasan virus baru dari sel terinfeksi. Seperti HA, NA
adalah glikoprotein, tapi tonjolan NA seperti
mushroom/jamur.
 Terdapat 16 antigen HA (H1-H16) dan 9 tipe antigen NA
(N1-N9), diantara ini hanya 4 subtipe HA (H1, H2, H3, dan
H5) dan 2 subtipe NA (N1 dan N2) yang telah menginfeksi
manusia
 Struktur Virus Influenzae

Gambar 2. Gambaran protein permukaan Hemaglutinin dan

Neuraminidase pada partikel virus influenza
 Replikasi Virus Influenzae

Gambar 3. Mekanisme replikasi pada virus influenza

 Variasi Genetik
Virus Influenzae khususnya Virus Infleunzae virus
A mempunyai kemampuan perubahan antigenik
pada protein HA dan NA. Terdapat 2 tipe
perubahan antigenik

1. Antigenic Drift : localized outbreak

Terdapat perubahan minor antigenik pada
hemagglutinin atau neuraminidase-nya saja atau
kedua-duanya.
- Variasi ini sewaktu-waktu bisa terjadi.
- Variasi minor antigenic terjadi karena point
mutasi pada gen dari Hemagglutinin dan
neuraminidase sehingga menghasilkan asam
amino pada protein.
3. Influenza – Antigenic Drift (Seasonal
Influenza)
 Variasi Genetik
2. Antigenic Shift : can widespread epidemic Infl.
Terjadi perubahan urutan nukleotida pada gen
yang mengkode protein permukaan virus
akibat terjadinya genetic reassotment.
- Keadaan ini menyebabkan perubahan major
pada hemagglutinin atau neuraminidasenya
yang tidak dapat diterangkan melalui mutasi
yang sederhana, tapi mungkin terjadi karena
rekombinasi antara human dan animal strain
dari influenzae virus A.
- Pada setiap varian yang baru, terjadi
penambahan antigen yang baru sedangkan
beberapa antigen yang lama masih tetap
dipertahankan
3. Influenza – Antigenic Shift (Pandemic
Influenza)
 VIRUS INFLUENZAE

Tipe-tipe Virus Influenza

1. Tipe A : Mutasi spontan Variasi

Labil
2. Tipe B : Mutasi jarang
Kurang stabil
3. Tipe C : Mutasi tidak ada
Stabil
Akibat Mutasi Perubahan Ag
Strain Baru
 VIRUS INFLUENZAE
Patogenesis
Drop. I. Per Inh

Nasofarings : - Neuramidase Envelop :- lipida

- H.A
- Enzim neuramidase
. Viskositas

. Merusak Sal.bawah ---- Paru-paru

Paru-paru
Nekrosis Komensal ---> Patogen
Viremia Patogen luar

Sifat Pneumotropik

Mutasi Pneumonia
Br. pneumonia
†
tu Anak-anak
 VIRUS INFLUENZAE
Patogenesis
• Is aquired by respiratory route  upper
respiratory tract.
• Virus multiplies in the epithe;ium  destroys
cilia  transient viremia – production
interferon  severe malaise.
• If infection of the lower resp. tract 
pneumonia – toxaemia – high mortality
• Strain of S.aureus cleaved HA (HA1 and
HA2)  enhances infectivity some strain of
influenza
 VIRUS INFLUENZAE

Gejala Klinik

- Masa tunas 2 - 3 hari

- Gejala A = B = C
* A lebih berat
* shivering, malaise. Hesdache, aching
limb, back.mild leukopenia
* severity is proporsional to age
Infeksi pada Wanita Hamil :
Trim. I : Abortus
Trim. II & III : Kelainan saraf
Trim. IV : Ibu dan Anak †
 VIRUS INFLUENZAE
Diagnosa

1. Isolasi
* BP : Apus / Air cucian tenggorok
* 1-3 hari sebelum / setelah gejala
* Intranasal pada Ferret ---> Gejala
= Manusia
* Intra Amnion Telur berembryo

2. Serologis : * HI
* CFT
 VIRUS INFLUENZAE

Epidemiologi
 Sporadis
 Endemis
Pandemis
Wabah terjadi secara periodik
Tipe A : 2 - 3 tahun
Tipe B : 3 - 6 bulan
1. Bertambahnya orang yang peka (kelahiran)
2. Berkurangnya orang yang kebal (kematian)
3. Bertambahnya orang yang klinis sembuh,
tetapi masih mengandung vir.Influenzae
sepanjang tahun (taa gejala)
Mutasi
 VIRUS INFLUENZAE

Pencegahan  Vaksinasi

Macamnya : 1. In aktif vaksin : Sinar UV

560C beberapa menit
Eter & Formalin
2. “Live attenuated vaccin”
Bahaya : * Mutasi
* Virulensi berubah

Tidak Rutin diberikan ok : - Sifat mutasi, Mahal, Produksi

terbatas, Taa “Stock” :
1. Polyvalen
2. Mengandung : * Vir. yang berjangkit di negara tetangga
* Vir. yang menyebabkan wabah terakhir
di negara yang bersangkutan
* Tipe virus lain : B atau C
 VIRUS INFLUENZAE

Pencegahan  Vaksinasi
* Hanya mencegah virus tidak menjalar
ke Saluran napas bawah
* Kekebalan  Lama kekebalan belum
diketahui
* Vaksinasi dikatakan berhasil :
- Belum mengadakan wabah di
negara yang bersangkutan
- Belum masuk ke negara
bersangkutan
 VIRUS INFLUENZAE

Pencegahan  Vaksinasi

Dilakukan pada orang yg memp.:

1. Risiko besar untuk dijangkiti
2. Risiko † bila dijangkiti, mis.:
- Penyakit kronis
- Wanita hamil
- Usia lanjut
- “Community services”
 Poliovirus
Enterovirus
Echovirus

Coxsackievirus
Picornaviridae
 Characteristic : see table
 Replication cytoplasm
 CPE : Virus crystallization in
cytoplasm
 To cause infected-host cell death
 Specimen from : respiratory tract.,
gastro intestinal tract., & blood.
 Viral growth on cell-culture :
human kidney cell, monkey, and
Hela cell.
 Virus characteristic :
- Inactive by heating at 55°C, 30 min. &
chlorine 0.01ppm, formaline & UV.
- Stable by added 1 mol/dl Mg2+.
- Can be found in milk, ice cream 
pasteurization.
- Based on antigenic differentiated in 3 type
:
Type I = Brunhilde  the most virulent
Type II = Lansing
Type III = Leon
• The disease can be mild illness, aseptic
meningitis to flaccid paralysis
Infection characteristic:
- Incubation period 1-2 weeks (sometime 5-6 week)
- Kind of infections :
1. Inapparent infection :
- Clinical sign (-).
- Virus can be isolated from feces.
- increased antibody titter.
2. Minor Illness : = poliomyelitis abortive
- Pharyngitis, fever; + diarrhea, + headache.
- Virus isolation : throat swab & feces.
3. Major Illness :
- Non paralytic poliomyelitis
- Paralytic poliomyelitis
- Clinical appearance biphasic  Dromedaris
fever.
*Diagnosis :
a. LCS examination
b. isolation : throat swab at initial of
infection and feces at late phase
c. serologic : Nt & Cf tests

* Preventing, treatment & Control

1.Immunization
2.Treatment symptomatic & rehabilitation
 VARICELLA-ZOSTER VIRUS (VZV)

– Varicella (chickenpox) :
 a mild, highly contagious disease
chiefly in children
 characterized clinically by a
generalized vesicular eruption of
the skin & mucous membranes
– The disease may be severe in adults &
immunocompromised children
 VARICELLA-ZOSTER VIRUS (VZV)

Zoster (shingles)
 a sporadic, incapacitating disease
of adults or immunocompromised
individuals
 characterized by rash limited to
distribution to the skin innervated
by a single sensory ganglion
 lesions similar to those of

varicella
 VARICELLA-ZOSTER VIRUS (VZV)
PROPERTIES OF VIRUSES

 VZV is morphologically identical to

HSV
 The virus propagated in cultures of
human embryonic tissue, produce
typical intranuclear inclusion bodies
 Cytopathic changes are more focal and
spread much more slowly than HSV
 VARICELLA-ZOSTER VIRUS (VZV)
PATHOGENESIS

 Varicella : route of infection is the mucosa

of the upper respiratory tract or
conjunctiva

blood multiple cycle of replication

skin
 VARICELLA-ZOSTER VIRUS (VZV)

Zoster
 skin lesion histopathologicaly
identical to varicella
 acute inflammation of the sensory
nerve & ganglia
 often only a single ganglion may be
involved
 as a rule the distribution of lesions
in the skin corresponds closely to
the areas of innervation from an
individual dorsal root ganglion
VARICELLA-ZOSTER VIRUS (VZV)
Varicella Herpes Zoster
 VARICELLA-ZOSTER VIRUS (VZV)
IMMUNITY

 Previous infection with

varicella is believe to confer
lifelong immunity to varicella
 However, zoster can occur in
the presence of relatively
high level of Nt Ab to varicella
 VARICELLA-ZOSTER VIRUS (VZV)

Laboratory diagnosis

 Stained smear of scraping or

swabs of the base vesicles :
multinucleated giant cells
 Virus isolated from vesicle fluid
using culture of human cells 3 – 7
days
 Cytopathic effects develop more
slowly
 VARICELLA-ZOSTER VIRUS (VZV)
Treatment

 Gamma globulin of high VZV Ab titer (VZ

Ig) can be used to prevent the
development of the illness of immuno-
compromised patients exposed to varicella
 It has no therapeutic value once varicella
has started
 Antiviral : acyclovir, valacyclovir,
vidarabine
Terima Kasih
RNA viruses positive
sense
RNA viruses negative
sense
Etiology of poliomyelitis, pleurodynia,
myocarditis, meningitis, encephalitis, & ARTI.
Pathogenesis
 Port of entry ; per oral  - droplet infection
- food & drink
- mechanic : fly,
cockroach, ant
Primary replication at oropharynx & GI tract.,
followed by viremia.
 Damage in CNS & muscle
 Local Ig A & Ig M/G formation after natural
infection