Infectious Diseases

(Virology)

Farmasi Ubaya S2 Oktober 2016

 Dr Ediyono Sp. P
 Sub Departemen Paru RSAL Dr Ramelan
 Infectious Diseases
Penyebab :
a. Infectiuos diseases : viral , ricketsial
b. Infectiuos diseases : bacterial, clamydial
c. Infectiuos diseases : spirocetal
d. Infectious diseases : protozoal, helminthic
e. Infectiuos diseases : mycotic
 Infectious Diseases
Sistim organ :
a. Skin infection
b. Wound infection.
c. Respiratory System infection ( Upper & Lower Resp ).
d. Digestive System infection ( Upper & Lower Digest ).
e. Genitourinary infection
f. Nervous System infection (Rabies)
g. Blood (cardiovasculer) and Lymphatic infection (Ebola)
h. HIV Disease and Complcation
 Basic Virology
• Struktur Virus
• Replikasi
• Genetik
• Klasifikasi Virus
• Patogenesis
• Pertahanan tubuh
• Diagnosis Laborat
• Obat Anti viral
• Virologi dalam Klinis
 Virus
 Virus : elemen genetik , replikasi tergantung dari sel host
 Parasit intrasel obligat (“Obligate intracellular parasites”)
 “Are not cell” (compl molecules : protein & nucleic acid )
 Replikasi virus  masuk kedalam sel host ( infection)
 Infeksi virus diikuti kerusakan sel host
 Menyebabkan Infeksi latent, kanker
Struktur
Virus
 Mophology mikroorganisme
Bacteria Cell

Rickettsia E. coli

Streptococcus

Poxvirus
Yellow Fever

Poliomyelitiis
Herpes simplex

Rabies
HIV Influenza Adenovirus
Adenovirus HIV

Bentuk Virus

Rabies Virus
Influenza Virus

Ebola Virus
 Morphology of Viruses

Complex Viruses Enveloped Viruses Naked Viruses

DNA Virus Herpes Virus Adeno Virus

Mumps Virus

Rhabdo Virus HIV Virus Papiloma Virus

 Fungsi Capsid & Envelop
• Pembungkus
• Pelindung asam nukleat terhadap pengaruh lingkungan
• Sarana penempel dan infeksi virus thd sel target
• Trigger terhadap bermacam-macam model infeksi
 Sifat spesifik virus
a) Hanya ada 1 tipe asam nukleat (DNA atau RNA)
b) Struktur sederhana : kapsid & asam nukleat
c) Tak ada informasi genetik untuk sintesa energy/protein
d) Replikasi dalam sel hidup
e) Asam nukleat virus mudah dipindahkan ke sel hidup lain
f) 1 virus replikasi  beratus-ratus progency virus

Radji M. Imunologi & Virtologi .1th.ed. PT ISFI Penerbitan Jakarta.2010

 Perbandingan bakteri, klamidia, ricketsia & virus
Bakteri Klamidia Ricketsia Virus
Parasit intra sel Tidak Yes Yes Yes
Membran Ya Ya Ya Tidak
plasma
Nucleic acid DNA + RNA DNA + RNA DNA + RNA DNA / RNA
Ribosom YA YA YA TIDAK
Peka pd YA YA YA TIDAK
antibiotika
Sensitif TIDAK TIDAK TIDAK YA
INTERFERON
Replikasi biner Ya YA YA TIDAK
 Stage of the viral growth cycle
1. Attachment & penetration by parenteral virion

2. Uncoating of the viral genome

3. Early viral mRNA – protein Synthesis

5. Viral genome replication

6. Late viral mRNA – protein synthesis

Virion release from cell

Viral Reproduction (Replication/Multiplikasi)
 Viral Reproduction (Replication/Multiplikasi)

1. Virus attaches to surface of susceptible cell by

specialized structures on specific receptors on the
cell surface

2. Virus enters cell by endocytosis (fusion of viral

membrane & cell membrane) or
lysis of cell membrane.
Morfologi virus RNA ( HIV )
Penempelan virus pada sel
Reseptor pada virus
Human Virus Avian Virus
 Sel Target HIV

Sel epitel usus

Diare, BB < Sel Otak
Lethargy, dementia

Sel Limfosit CD4

Makrofag

Kontrol antibodi
 Cara Penetrasi virus dalam sel
A, Endocytosis & uncoating : Herpes virus

B, Fusion of cell membrane with viral envelope : Mumps virus

Replication of Positif sense
Single stranded RNA virus
Umumnya virus tidak masuk ke inti sel

1. Penetrasi & pelepasan RNA virus

2. RNA diterjemahkan pada host sel.

3. Sintesa gen

4. Sintesa RNA positif

5. RNA + protein  virus matur.

 Genetic stage in the
multiplication of ds DNA virus
Virus penetrasi ke host sel 
melepaskan DNA

1. Masuk ke inti sel

2. Terjadi transkripsi
3. Viral mRNA diterjemahkan pada
struktur protrein masuk ke inti
4 . Replikasi virus DNA di inti sel
5. Viral DNA & protein  Virus matur
6. Viral DNA menempel DNA host
 Infeksi Latent
( HIV, Hepatitis B )

6. Viral DNA menempel

pada DNA host
 2 Binding dan Fusion
1 Virus bebas Virus mengikat CD4 pada
1 dari 2 koreseptor (CCR5 dan CXCR4),
& melebur dengan sel
S
3 Infeksi Reseptor CD4
I
K Virus menembus sel Koreseptor CCR5
L mengosongkan isinya RNA HIV
Koreseptor CXCR4
ke dalam sel DNA HIV
U
S 4 Reverse Transcription DNA man
ssRNA diubah menjadi
dsRNA oleh enzim DNA HIV 6 Transkripsi
H reverse transcriptase Pembentukan protein
I DNA man
rantai panjang
D 5 Integrasi
DNA virus menyatu
U
dg DNA sel oleh 8 Budding
P enzim integrase Virus immatur
mendorong ke luar,
H
7 Assembly mengambil sel membran
I Pembentukan rantai protein virus
V

10 Maturasi 9 Virus immatur keluar

dari sel terinfeksi
 Skema fase multiplikasi virus dalam sel hospes

1000

100

10

1 2 3 4 5 66 77 88 99 10
10 Jam
 Viral Growth Curve
 1 Virion ( 1 partikel virus ) yang menginfeksi sel  replikasi
dalam 10 jam  beratus Virion

 Replikasi HIV yg cepat (107 partikel infeksius

/mm3 per hari)

G
E Viral Nucleic Acid
N
E (+) ss DNA
T Single-
stranded
I DNA (-) ss DNA
K Double-
stranded
Virus (+) ss RNA
Single-
stranded
RNA Double-
(-) ss RNA
stranded
Sintesa Protein DNA

Penyalinan Informasi
Genetik Trancription

mRNA rRNA tRNA

Ribosome
Terjemahkan informasi
Translation Genetik menjadi polipeptida-
Asam amino

Protein
 DNA Viruses
Klasifikasi Virus

Smallpox virus
Vaccinia virus
Molluscum contagiosum
 RNA Viruses

Virus HIV

Enterovirus
Rhinovirus
Virus Flu, mumps Hepatitis A
Reovirus
Ritavirus

Virus Influenza A&B Virus Rabies

Hanta Virus Hepatitis E
Norovirus
Virus Ebola

SARS
 Klasifikasi virus

• Virus saluran  Virus saluran  Arbovirus

pencernaan pernafasan ( ditularkan lewat
( enteric virus ) ( respiratory virus arthopoda )
)

 Rotari virus  Orthomycovirus  Orbivirus

 Coronavirus  Rhinovirus  Flavivirus
 Enterovirus  Coronavirus  Rhabdovirus
 Adenovirus  Adenovirus  Bunyavirus
 DNA Virus
Family Genus virus Genus member Penyakit

DNA Variola & Smallpox,

Poxviridae Variola & Vaccinia
VIRUS Vaccinia cowpox

Herpes simplex
Fever blister
Simplex (HSV) 1
virus Herpes simplex
Genital herpes
(HSV) 2
Herpes
viridae Varicella shingles
Varicella zoster
virus ( " dap “)

Cytomegalo
Human CMV CMV infection
virus
 DNA Virus ( lanjutan )
Family Genus virus Genus member Penyakit

Adeno- Mastadeno- Human Adenovirus

viridae virus adenovirus infection
Papiloma
HPV Warts
virus
Papova-
DNA viridae Polyoma- Leuko-
JC virus
VIRUS virus encephalopathy

Hepadna- Hepadna-
Hepatitis B virus Hepatitis
viridae virus

Parvo- Erythema
Erythrovirus Parvovirus B19
viridae infectiosum
 RNA Virus ( 1)
Poliovirus Polyomyelitis
Enterovirus
Coxsackie virus Hand-footmouth disease
Picornaviridae
Hepatovirus HAV Hepatitis A

Rhinovirus rhinovirus Common cold

Calciviridae Calcivirus Viral diarhea

Alphavirus Encephalitis virus Encephalitis

Togaviridae
Rubella
Rubivirus Rubella virus
( German measles )

Flaviviridae Flavivirus Dengue fever virus Dengue Fever ( DHF )

Filoviridae Filovirus Ebola virus Ebola fever

 RNA Virus (2)
Orthomyxoviridae Influenza virus Virus Flu type A Flu, Avian Influenza

Paramyxoviridae Para influenza Para influenza

Paramyxovirus

Mumps virus Mumps ( Parotitis )

Morbilivirus Measles virus Measles ( Morbili )

Rhabdoviridae Lyssavirus Rabies virus Rabies

Retroviridae Oncornavirus HTLV T-cell Leucemia

Lentivirus HIV 1 , 2 AIDS

Coronaviridae Coronavirus SARS ARDS

 DNA Enveloped viruses
SMALLPOX

Gambaran klinis
 Virus masuk ke sal nafas atas  kelenjar limfe  Darah ( viremia )
 Inkubasi : 7 – 14 hari
 Gejala prodromal : demam, lemah badan
Cowpox virus
 Fever Blisters or Cold Sores.
Herpes Simplex Virus ( HSV-1 )
 Genital Herpes
Herpes simplex (HSV) 2

Shingles, or
herpes zoster
Genotipe Human Papiloma Virus
Genital warts
Figure 6 A-D: Example of foot warts:
Erythema Infectiosum
(Fifth Disease)
 Hand-Foot-Mouth
Poliomyelitis Disease
 Hand, Foot and Mouth Disease
– spread by oral-fecal route
– Malaise, headache and abdominal pain, followed by sores on tongue, buccal
mucosa and soft palate
– Maculopapular rash on hands, feet and buttocks
– Bullae on soles and palms
– ssRNA virus
 Rubella
( German Measles )

Measles ( rubeola )
 Mumps
( Parotitis )

- Dewasa  parotitis.
- Post-pubertal males 
orchitis, sterility.
- Komplikasi mumps :
meningitis and encephalitis
Rabies
 Patogenesis Infeksi Virus

 Cara masuk virus kedalam tubuh

 Replikasi pada lokasi infeksi

 Penyebaran virus & multiplikasi pada organ

 Diseminasi virus secara sistemik ke organ lain

Radji,M. Imunologi dan Virologi. Cetakan pertama. PT ISFI. Penerbitan Jakarta. 2010
 Jalan virus masuk-keluar dari
permukaan tubuh
1. Saluran pernafasan (udara)
2. Saluran pencernaan (bahan terkontaminasi).
3. Konjungtiva.
4. Kulit (luka lecet , gigitan binatang)
5. Pembuluh darah
6. Saluran urogenital
7. Artropoda.
8. Placenta
 Pintu masuk virus patogen
Pintu Infeksi Virus Jenis Penyakit
Influenza virus Influenza
1. Saluran
Rhinovirus Common cold
nafas
Respiratory syncytial virus Brochiolitis
Epstein barr - virus Inf – Mononucleosis
Varicella zoster virus Chicken pox
Herpes simplex virus tipe I Herpes labialis
Cytomegalovirus Mononucleosis syndrom
Measles virus Measles
Mumps virus Mumps
Rubella virus Rubella
Hantavirus Pneumonia
Adenovirus Pneumonia
 Pintu masuk virus patogen

Pintu Infeksi Virus Jenis penyakit

2. Hepatitis A virus Hepatitis A
Gastrointestinal
- tract Polio virus Poliomyelitis
Rotavirus Diarrhea
 Pintu masuk virus patogen

Pintu Infeksi Virus Jenis penyakit

3. Conjungtiva Rabies virus Rabies
Yellow fever Yellow fever
virus
Dengue virus Dengue
Human Papilomas
papiloma virus ( Warts )

Conjunctivitis
 Pintu masuk virus patogen

Pintu Infeksi Virus Jenis penyakit

4. Skin Rabies virus Rabies
Yellow fever Yellow fever
virus
Dengue virus Dengue
Human Papilomas
papiloma virus ( Warts )
 Pintu masuk virus patogen
Pintu Infeksi Virus Jenis Penyakit
5. Blood Hepatitis B virus Hepatitis B
Hepatitis C Hepatitis C
Hepatitis D Hepatitis D
HIV AIDS
Cytomegalovirus Mononucleosis
syndrome /
Pneumonia
Human T-cell Leukemia
lymphotropic virus
 Pintu masuk virus patogen

Pintu Infeksi Virus Jenis Penyakit

6. Genital – Human Papilomas
tract papiloma virus ( Warts )
Hepatitis B virus Hepatitis B
HIV AIDS
Herpes simplex Herpes genitalis
virus tipe 2
 Pintu masuk virus patogen

Pintu Infeksi Virus Jenis Penyakit

8.Transplacenta Cytomegalovirus Congenital
abnormality
Rubella Congenital
abnormality
 Target Organ Virus
Central Nervous system Eye
- HSV, VSV, CMV
- HSV, Herpes, CMV
- Vaccinia virus
- JC virus
- Adenoviruses
- Rabies virus, Arbovirus
- Enterovirus
- Mumps and Measles virus
- Rubella virus
- Enterovirus

Liver
Parotitis - HAV, HBV
- Mumps virus - EBV, CMV, HSV
- NonA-nonB hepatitis
- Yellow fever virus
- Ebola virus
Upper Resp tract
- HSV, HBV, adenovirus
- Coxsackievirus A Skin
- Rhinovirus, Influennza virus - HSV, VSV,poxviruses
- Measles, RSV, coronavirus - Papiloma virus
- Measles, Rubella
- Coxsachi
Lower Resp tract
- VZV, CMV, adenovirus
- Coxsackievirus A Embryo
- Rhinovirus, Influennza virus - HSV, CMV, VSV
- Measles, RSV, coronavirus - Rubella virus

Digestive tract Bladder

- Rotari virus - Adenovirus (Hemorhagic cystitis)
- Enteric-adenoviruses
- Astroviruses
- Enteric coronavirus Genital Organ
- HSV, Papiloma virus
 Patogenesis Infeksi Virus
Tropisma Virus :
 Tropisma virus : Sifat virus yang dapat mengenali
dan menempel pada permukaan sel jaringan tertentu
Polio virus Sel saraf tertentu
HIV CD4 sel T
Rhinovirus Saluran nafas (ph rendah, O2 tinggi)
Enterovirus Usus
Virus rabies Sel saraf
Virus hepatitis B Reseptor albumin pada sel hati
Virus Epstein-Barr Reseptor CD21 (sel limfosit B)
 Aspek Kinetik Infeksi Virus
 Penularan virus dapat lewat darah .
 Lebih sering lewat saluran limfe ( ok mudah dicapai ).
 Umummnya virus menginfeksi sel darah putih.
 Eritrosit tak dapat diinfeksi oleh virus (Tak ada bahan untuk
metabolisme virus ).
 Virus yang mampu menginfeksi neuron ( neurotropic viruses) dapat
berjalan sepanjang saraf dari perifer ke saraf pusat.
 Virus rabies : dari tempat gigitan ke saraf pusat lewat saraf sensori
 Virus dapat menular ( Placenta ) dari ibu ke janin
 Akibat Infeksi Virus pada sel

1. Efek Sitopatogenik
2. Inhibisi makromolekul sel hospes
3. Inhibisi sintesis DNA, RNA & Protein
4. Kerusakan lisosom sel hospes  kerusakan sel
5. Virus mengekskresi Toxin – kerusakan sel
6. Peleburan (fusi) sel
 Akibat Infeksi Virus pada sel

1. Efek Sitopatogenik
Contoh: Hospes
Adeno virus, Herpes Sel bengkak

Picornavirus Lysis sel saat virus keluar

(Rhinovirus, hepatitis A)

Paramyxovirus Sel berinti banyak

( Flu virus, Mump)
 Akibat Infeksi Virus pada sel

2. Inhibisi makromolekul sel hospes

Partikel virus  gen-gen virus tak lengkap(“detective interfering particle”)
 Menghambat sintesa makromolekul (karbohidrat, lemak, asam nukleat &
protein

3. Inhibisi Sintesis protein

Poliovirus
Herpesvirus
Paramyxovirus
Adenovirus
 Kematian sel ok virus
 Inhibisi sintesa protein (importance effect)
 Inhibisi DNA / RNA sintesa (secunder effect)

Inhibisi

Initiation Celluler Celluler

Poliovirus
factor mRNA Protein

Kerusakan sel saraf

 Kerusakan saraf
akibat polio
Virus Polio masuk
tubuh

Masuk dalam sel

lewat reseptor

Replikasi di
sitoplasma

RNA virus gabung

dalam ribosom

Sintesa RNA &

Protein host
dihambat
Poliomyelitis

Virus Polio
 Kelainan Sel Hospes ok Replikasi Virus

3. Inhibisi Sintesis RNA

Poliovirus menghambat sintesis r-RNA : 90 menit

Adenovirus menghambat sintesis r-RNA : 8-10 jam

4. Inhibisi Sintesis DNA

Penurunan sintesis DNA: 4 jam setelah infeksi

Biasanya virus menghambat sintesis protein dahulu
 Interaksi Virus pada Host cells
Virion
Infection

Host cell
Disease of host cell Genetic alteration
of host cell

Productive Infection
More virus produced LATENT STATE
Nucleic acid of virus becomes
Part of host cell DNA or
Lysis of cell- Release of virions- Replicates as a plasmid
Release of viruses Non-lysis of cell

Host cell multiples- Host cell is often modified

Host cell dies Continuous leakage And continues to multilple
Of virions
 Akibat Infeksi Virus pada sel

Burkit’s Lymphoma

Transformasi Infeksi akut Latent /

Proviral Persisten /
( Onkogenik ) ( Sel lisis )
( sel ada gen virus ) Kronis /
Virus herpes, Slow
Epstein Barr ( Hepatitis B, HIV )
Keganasan
A Time course of appearance of disease symptoms and infectious virions of viral infection
Tahapan penyebaran virus dalam hospes

1. Virus masuk lewat pintu masuk kedalam tubuh

2. Replikasi lokal dan penyebaran lokal

3. Penyebaran virus lewat pembuluh darah

4. Multiplikasi virus pada organ sasaran

5. Infeksi kongenital
 Tahapan penyebaran virus dalam hospes

1. Virus masuk
lewat pintu masuk
kedalam tubuh
 Penyebaran Virus dalam Hospes

• Penyebaran lokal pada epitel.

• Penyebaran lewat saluran limfe.

• Penyebaran virus lewat darah.

• Penyebaran lewat sistim saraf.

Penyebaran lokal pada epitel
Penyebaran lewat sistim saraf.
 Tabel 7.1. Virus yang dapat menyebar keseluruh tubuh
Jenis penyakit Pintu Masuk Rute perjalanan Organ sasaran
Hepatitis A Saluran Cerna Darah Hati
AIDS Injeksi, trauma, Darah Limfosit T, Otak
anogenital
Rubella Saluran Nafas Darah Kulit, Limpa, Janin
Measles Saluran nafas Darah Kulit Paru, Otak
Cacar air Saluran Nafas Darah Kulit, Paru
Arbovirus Kulit (gigitan nyamuk) Darah Otak, sel darah
Hepatitis B Kulit, injeksi Darah Hati
Poliomyelitis Saluran cerna Darah, Saraf Sistim saraf Pusat
Herpes simplex – 1 Saluran nafas Saraf, lekosit Kulit, Otak, Hati
Rabies Kulit (gigitan hewan) Saraf Otak
Herpes simplex – 2 Saluran genital Saraf Saluran genital
5. Infeksi kongenital ok virus

CYTOMEGALOVIRUS ( CMV )
5. Infeksi kongenital ok virus

Rubella
Tabel 7.2. Virus persisten pada manusia

Measles Subacute sclerosing panencephalitis

Rubella Encefalitis progresif

Papovavirus Multifokal leukoencefalitis progresif

HIV Aids dementia complex

Echovirus Kelainan mental

 Virologi Diagnostik
• Laboratorium

1) Isolasi virus
2) Penemuan langsung virus
3) Asam nukleat virus
4) Pemeriksaan antigen
5) Tes serologis antibodi spesifik

Johnson AG, Zieger RJ, Hawley L. Essential Mikrobilogi dan Imunologi. Edisi ke-5. Binarupa Aksara. 2011
 Virologi Diagnostik

1. Bila gejala klinis khas : tak perlu laboratorium

2. Pemeriksaan dengan mencari penyebab yang

paling mungkin

3. Pada beberapa hari pertama sulit dilakukan

Johnson AG, Zieger RJ, Hawley L. Essential Mikrobilogi dan Imunologi. Edisi ke-5. Binarupa Aksara. 2011
 Viral Isolation/ Cultur

• “Gold standard”

• Three methods

– Cell culture

– Animal inoculation

– Embryonated eggs
VIRAL PATHOGENESIS
AND ASSOCIATED
DISEASES
Infeksi Virus dalam Klinis (Organ)

1. Saluran nafas
2. Sistim saraf
3. Hati
4. Saluran cerna
5. Kulit dan Mata
6. Limfatik dan Kardiovaskuler
7. Virus penyebab tumor
 1. Infeksi Virus pada Saluran nafas

a. Virus Influenza
b. Virus Flu Burung ( Avian Flu-H5N1)
c. Virus Flu Babi ( H1N1)
d. Virus Parainfluenza
e. Respiratory Syncytialvirus (RSV)
f. Human Metapneumovirus (HMPV)
g. Adenovirus
h. Rhinovirus
i. Coronavirus
j. Virus SARS
 Influenza Virus
• Virus famili orthomyxoviridae

• Virus Influenza : Tipe A,B,C

• Virus Influenza A : Unggas, Babi & Manusia

• Virus Influenza B : Manusia

• Virus Influenza C : Babi & Manusia

Influenza B dan C hanya dapat menimbulkan
sakit ringan dan tidak menyebabkan epidemik
Latest Update on A New Influenza Viral H1N1 ( Swine Flu) , PERSI, 13 Juni 2009
 VIRUS INFLUENZA
• Perbedaan H dan N merupakan dasar subtipe
H (1 - 15 ) dan N ( 1 – 9 )
• Virus tsb dapat diidentifikasi pada manusia, babi, kuda
dan unggas ( avian)
• Virus Influenza pada manusia : H1N1,H2N2, H3N2, dan
virus avian ( H5N1)
• H5 ditemukan pada ayam 1959
• Pada unggas ditemukan 1878 di Itali
File:Influenza Nomenclature Diagram
Morfologi & Struktur Virus
 Kategori influenza A berdasarkan struktural
glikoprotein di permukaan virus :
HEMAGGLUTININ (H)
Fungsi menempelkan virus ke reseptor sialic acid pada permukaan sel manusia  RNA virus
masuk nukleus  membentuk virus baru
NEURAMINIDASE (N)
Fungsi membawa virus baru dari sel host ke sel-sel lain lewat saluran pernafasan.
Influenza tipe A dikategorikan berdasarkan variasi struktur dari 2 glycoprotein, hemagglutinin (H) dan
neuraminidase (N) pada permukaan virus.
Fungsi dari hemagglutinin adalah menempelkan virus influenza ke reseptor sialic acid di permukaan sel
manusia. Setelah berikatan, sel flu masuk ke dalam sel host, kemudian RNA virus masuk ke nukleus sel.
RNA virus kemudian membentuk partikel-partikel virus baru.
Sedangkan fungsi dari neuraminidase adalah sederhana tapi penting. Yaitu memungkinkan virus yang baru
terbentuk untuk berpisah dari sel host dan dapat berjalan bebas dari satu sel ke sel lainnya lewat saluran
pernapasan.
 Pengertian
• Flu Burung ( Avian Flu, AI ):
Infeksi yang disebabkan oleh Virus Influenza A subtipe H5N1, yang pada umumnya
menyerang unggas.
- Dari unggas ke unggas, hewan lain dan manusia.
- Penularan dari manusia ke manusia belum terbukti.
- Melalui kotoran atau sekreta unggas, mencemari udara dan tangan penjamah.

• Flu Babi ( Swine Flu ):

Infeksi yang disebabkan oleh Virus Influenza A subtipe baru H1N1-Strain Mexico
pertama dideteksi April 2009.
- Manusia ke manusia ( Batuk, bersin )
- Benda tercemar virus  mulut, hidung
 Kelompok resiko tinggi Avian Flu
 Pemilik & pekerja di industry peternakan ayam
 Pekerja pemotong dan pengolah bahan baku daging
ayam
 Sopir kendaraan pengangkut ayam
 Pengusaha catering
 Petugas laboratorium yang menangani spesimen
pasien flu burung / hewan sakit
 Petugas kesehatan, keluarga yang merawat, atau
yang kontak erat dengan pasien flu burung

Nasronudin. Aspek Molekuler Avian Influenza. Penyakit Infeksi di Indonesia & Solusi Kini Mendatang. Edisi ke-2. 2011, hal 82-5.
 Kelompok resiko tinggi
• Petani, pekerja peternakan, petugas pemroses
produk-produk peternakan (jagal, pedagang)
• Petugas yang terlibat pada pembantaian, transport,
atau pembuangan limbah peternakan yang terinfeksi
flu burung
• Petugas laboratorium yang menangani spesimen
pasien flu burung / hewan sakit
• Petugas kesehatan, keluarga yang merawat, atau
yang kontak erat dengan pasien flu burung

Laksmi Wulandari, 2005

 Cara Penularan Avian Influenza

• Cairan/ lendir yang berasal dari lubang hidung, mulut, mata

(konjungtiva), dan lubang anus (tinja) dari unggas yang
sakit ke lingkungan.
• Kontak langsung dengan ayam sakit.
• Secara tidak langsung melalui pakan, air minum, pekerja
kandang, dan peralatan peternakan, rak telur, keranjang
ayam dan alat transportasi yang tercemar AI.
• Unggas air yang berperan sebagai reservoir virus AI
melalui virus yang ada pada saluran intestinal dan
dilepaskan melalui kotoran.
(www.cdc.gov/flu/avian/gen-info/facs.htm)
 Mutasi genetik virus Influenza
• Virus mampu mengubah sifat
antigen selaput glikoprotein
“Antigenic drift “ & “Antigenic shift”

• Keduanya merupakan cara virus

untuk menyesuaikan diri terhadap
lingkungan atau inang barunya
Antigenic drift
 Antigenic shift
• Terjadi bila 2 strain virus secara simultan
menginfeksi sel inang yang sama rekombinasi
segmen RNA virus baru

• Babi dianggap inang perantara yang penting. Trakea

babi memiliki reseptor baik untuk virus manusia &
virus unggas
 Jump directly from birds
to human without
undergoing genetic change

The new strain

may further
evolve to spread
from person to
person. If so, a
Human influenza A flu pandemic
strain
could arise.

Bird influenza A
strain

Jump directly The new strain

from birds to can spread
animal host and from the
then to humans intermediate
without host to humans
undergoing
genetic change
 Gejala Klinis “ Swine flu “:
Inkubasi : 1- 5 hari Nyeri otot
Batuk Mual
Demam Nyeri perut
Lemah Badan Diare
Nyeri kepala Sesak nafas
Nyeri telan Nyeri sendi
Pilek
Kedinginan
 Comparison
Human Avian Swine

Etiology H1N1 H5N1 H1N1

Epidemiology Seasonal Pandemic Pandemic
threat phase 6
Transmission Human to human Animal to human Human to human

Morbidity High Low High

Clinical picture usually mild Similar to human, Similar to human,
Many severe fatal usually mild

Mortality Low High Low ?

Treatment Oseltamivir Oseltamivir Oseltamivir103
 SARS
• Severe Acute Respiratory Syndrome
 Penyebab: Corona Virus,
 sifatnya unik karena dapat
memindahkan informasi genetik antar
spesies.
 Mudah penyebaran pada kondisi
lingkungan buruk, sanitasi dan higiene
yang buruk, kontak dengan burung
atau babi memudahkan penyebaran
virus.
• Gejala SARS : demam, sesak dan
gejala respiratoris lain.
• BAHAYA: cepat menjadi pneumonia
berat dan menimbulkan ARDS dalam
minggu ke 2 perjalanan penyakit
• ARDS bila PAO2/ FiO2 < 200
ARDS
• Antiviral Drugs and H1N1 Flu (Swine Flu)

1. Oseltamivir,
2. Zanamivir, Oseltamivir

3. Amantadine
4. Rimantadine
Table :. Antiviral dosing recommendations for treatment or
chemoprophylaxis of novel influenza A (H1N1) infection.
IDSA guidelines for seasonal influenza.

Agent, group Treatment Chemoprophylaxis

Oseltamivir ( Tamiflu )

75-mg twice per day 75-mg / day

Adults for 5 days

15 kg or less 60 mg / day divided 30 mg / day

into 2 doses

16-23 kg 90 mg / day divided 45 mg / day

into 2 doses
Children ≥ 12
months 24-40 kg 120 mg/ day divided 60 mg / day
into 2 doses

>40 kg 150 mg / day divided 75 mg / day

into 2 doses
 Adenoviruses
Penyakit
 Infeksi saluran nafas atas :
- Pharingitis
- Pharyngoconjungtivitis
- Bronchitis, Atypical Pneumonia
 Hemorhagic cystitis ( kencing sakit, berdarah )
 Gastroenteritis ( diarhe tanpa darah – pada anak )

GEJALA KLINIS
1. Infeksi umumnya ringan DIAGNOSTIK
2. Gejala : Demam, batuk, pilek, sesak wheezing 1. Electron microscopy
3. Berat  Pneumonia 2. Virus Antigen
4. Lekosit meningkat 3. Viral DNA
5. CRP( C-Reactive Protein) meningkat 4. Culture
5. Serology
 2. Infeksi Virus pada Sitem Saraf

a. Virus Rabies
b. Arbovirus Encephalitis
c. Virus Polio
d. Coxsackievirus
e. Echovirus
f. Spongiform Encephalopathy
 RNA Enveloped viruses
RHABDOVIRUSES

 Rabies virus
 Masa Inkubasi
Rabies

Gigitan di kepala ± 30 hari

Radji,M. Imunologi dan Virologi. Cetakan pertama. PT ISFI. Penerbitan Jakarta. 2010
 Rabies
GEJALA KLINIS :
• Gejala rabies muncul  penyakit hampir pasti FATAL.
• Virus  kerusakan saraf sentral (Otak, medula spinalis )
• Pencegahan : perawatan sebelum gejala muncul.
• Gejala terjadi : dalam 4 – 6 minggu.
• Gejal awal:
- Nyeri
- Demam
- Batuk , nyeri tenggorokan
- Rasa terbakar, gatal, bingung
- Nyeri perut.
- Cemas, gelisah, bingung.
 Rabies
Gejala Klinis
• Stadium lanjut:
- Cemas, binung, gelisah
- Halusinasi
- Delirium
- Hydrophobia (Takut air) or aerophobia (takut udara).
- Spasme otot muka, leher, diafragma
- Paralysis (often associated with rabies from vampire
bats)
- Koma, Gagal nafas, gagal jantung.
• Hydrophobic spasm of inspiratory muscle
 Poliomyelitis
 3 serotype poliovirus : PV1, PV2 & PV3
 Poliovirus tipe -1 ( PV1 ):
- paling sering didapatkan,
- menyebabkan paralysis ( lumpuh ).
 Vaksin Polio  Immunity ↑  Replikasi virus (-)  penyebaran virus dicegah

TRANSMISSION
• Spreads easily from human-to-human contact
• Primarily via the fecal-oral route
• Ingesting contaminated food or water
• Incubation period, is usually 6 to 20 days
• Replikasi di Usus  darah – sel epitel usus & saraf
• Sebagian besar kasus infeksi pada bayi, anak-anak
• Gejala klinis sangat bervariasi :paralisis , poliomielitis, meningitis,
 3. Infeksi Virus pada Hati

a. Virus Hepatitis A
b. Virus Hepatitis B
c. Virus Hepatitis C
d. Virus Hepatitis D
e. Virus Hepatitis E
f. Virus Hepatitis G
g. Virus Hepatitis TT
Virus Hepatitis
 Hepatitis Viruses
• Hepatitis A (HAV) – oral-fecal
• Hepatitis B (HBV) – blood and body fluids
• Hepatitis C (HCV) – blood and body fluids
• Hepatitis D (HDV) – blood and body fluids; requires HBV for replication
• Hepatitis E (HEV) – oral-fecal
STRUCTURE OF HBV
• Envelope containing
• HBsAg
• DNA polymerase
• Double-stranded DNA
• Single-stranded DNA
• HBcAg (HbeAg)
 Schematic Representation of HBV

DNA-polymerase HBV-DNA

Outer lipid envelope

containing
Inner protein HB surface antigen
core (HBcAg)

The infectiousHBeAg
HBV virion contains partially double-stranded DNA, a DNA
HBsAg
polymerase, a core antigen (HBcAg) and an ‘e’ antigen (HBeAg). Surface
antigen (HBsAg) is produced in large amounts and is a key marker of infection.
 Hepatitis Akut

konvalesen
a) 1-2 bulan (HAV)
Ikterik b) 3-4 bulan
( HBV/HCV)
a) 95% kasus
Preikterik b) gatal (10%)
a) Demam c) Hepatomegali (70%)
b) Mual d) Splenomegali (20%)
c) Muntah e) SGPT/SGOT ↑ (40-
d) Nyeri sendi 100 kali Normal)
e) Sakit Kepala f) Bulirubin ↑ (20 kali)
g) 2-12 minggu
 Virus Hepatitis A
- Penularan : saluran cerna
- Cara penularan : fekal-oral 4-15 minggu
- Inkubasi 2-6 minggu
2-3 minggu
Pemulihan
3 -12 hari a) gejala reda
Ikterik b) Nafsu makan baik
a) urine gelap c) Sembuh total
Prodromal b) Nyeri perut kanan
a) kelelahan
c) Bilirubin >
b) mialgia d) Splemomegali
c) mual, muntah e) gatal
d) nyeri perut kanan atas
e) demam
 4. Infeksi Virus pada Saluran Pencerrnaan

a. Rotavirus
b. Calicivirus
c. Torovirus
d. Adenovirus
 Acute Gastroenteritis Viruses
Characteristic Norovirus ( Sapovirus Rotavirus Astrovirus Enteric
Calicivirus) adenovirus
Age group All age Children 6-24 month <7 years <4years

Transmission Person-to- Person-to- Person-to- Person-to- Person-to-

person, person, person, person, person
water, water, cold water, food. water, food.
food, food,
shelfish shelfish
Outpatient 10-25 1-10 5-10 7-8 4-8
prevalence
In pateint Rare 3-5 35-40 3-5 5-20
prevalence
 Characteristic of Gastroenteritis virus infections
Sign Norovirus Sapovirus Rotavirus Astrovirus Enteric
&symptom adenovirus
Prodrome 1-2 1-3 1-3 3-4 8-10

Diarrhea 66-95% 88-95% 96-100% 72-100% 97%

watery

Vomitus 57-96% 44-65% 80-90% 20-50% 79%

Fever 24-48% 18-34% 60-65% 20% Occasionally

Low grade low grade
Abdominal Cramps - Colicky 50%
pain
Dehydration -1% Infrequent Frequent in In frequent Infrequent
youg
 4. Infeksi Virus pada Saluran Pencerrnaan

 Penyakit terbesar ke-2 setelah penyakit

saluran nafas ok virus
 Penyebab kematian pada anak-2 dan bayi
 Gejala utama :
a. Diarhea
b. Demam
c. Mual, Muntah
d. Malise
e. Nyeri dan kejang abdominal
 5. Infeksi Virus pada Kulit dan Mata

a. Virus cacar (Poxvirus)

b. Virus Herpes
c. Virus Herpes Simplex
d. Virus Varicella Zoster
e. Virus Campak
f. Vurs Rubella
g. Human Papilomavirus
 DNA Enveloped viruses
VARICELLA-ZOSTER VIRUS

Penyakit
 Varicella ( chickenpox )
 Zoster ( shingles )

 Penyebaran : - Droplet saluran nafas

- Kontak langsung
- Vertikal
 DNA Enveloped viruses
SMALLPOX

Gambaran klinis
 Virus masuk ke sal nafas atas  kelenjar limfe 
Darah ( viremia )

 Inkubasi : 7 – 14 hari

 Gejala prodromal : demam, lemah badan

 Chickenpox ( Varicella )

 Inkubasi : 14 – 21 hari
 Gejala :
- Demam
- Lemah badan
- Rash papulovesiculer dari leher
menyebar ke kepala dan ektremitas
-Rasa gatal
 Komplikasi : Pneumonia, Encephalitis, Reye Syndrome ( encepahlopathy, liver degenerasi )
Smallpox
 RNA Enveloped viruses
PARA - MYXOVIRUS

 Measles virus (Campak=Rubeola)

 Mumps virus (Parotitis)

 Respiratory syncytial virus

 Parainfluenza virus
 Measles ( Rubeola = Campak)
1) Virus masuk lewat saluran nafas  jaringan limfoid  darah (viremia)  sel epitel
permukaan tubuh Kulit, Saluran nafas, conjungtiva.
GEJALA KLINIK
Mudah menular, Inkubasi : 9-14 hari, DemaM, Malaise, Nyeri otot, Batuk, bersin, hidung
tersumbat, Mata merah, konjungtivitis, fotofobia

KOMPLIKASI
- Bronkitis
- Pneumonia
- Ensefalomielitis
- Kematian
- 10% wanita hamil dengan campat  keguguran
Ruam kulit mulai dari belakang
Telinga – menyebar ke seluruh tubuh.
Koplik spot pada rongga mulut
 Measles ( Rubeola = Campak)

1) Terapi - Preventif

- Tirah baring
- Antipiretik
- Vaksinasi pada anak < 9 bulan
- Vaksin MMR (mumps, measles, rubella)
 Rubella
GEJALA KLINIK
- Bisa pada bayi, anak, remaja atau dewasa
- Demam pada bayi
- Nyeri sendi pada dewasa
- Pembesaran kelenjar getah bening dari belakang kepala, belakang telinga,
leher bagian belakang dan rasa nyeri

Virus masuk lewat saluran nafas  kelenjar getah bening lokal  limfadenopathi 
viremia  Kulit, sal. Nafas, darah
 Rubella
• Complication
– arthritis
– thrombocytopenia
– meningoencephalitis
• Treatment: supportive
• Isolation:
– droplet precaution for 7 days after onset of rash,
– contact precaution for congenital rubella until > 1 yr-old
• Prevention: immunization
 Herpesviruses
Penyakit
 Latent infection : persisten infection

 Reactivation : from latent infection, asymptomatic

 Recurrence : reactivated virus  clinically obvious

 Herpesviruses
Ada 8 human herpersviruses
1 Herpes simplex virus 1 HSV-1
2 Herpes simplex virus 2 HSV-2
3 Varicella-Zoster VZV
4 Epstein-barr virus EBV
5 Cytomegalovirus CMV
6 Human herpesvirus 6 HHV-6 (HHV-6A & HHV-6B)
7 Human herpesvirus 7 HHV-7
8 Human herpesvirus 8 HHV-8
Herpes Simplex Virus

Mulut, Mata,
Type-1 (HSV- Saraf
1)
Herpes
simplex virus
Type-2 (HSV-
2) Saluran
Genital
 Herpes Simplex Virus HSV-1

Penyakit
1) Gingivostomatitis

2) Herpes labialis

3) Keratoconjungtivitis

4) Encephalitis

5) Diseminated infection ( esophagitis, Pneumonia )

Cold sore (Herpes
labialis) Keratoconjungtivitis
 DNA Enveloped viruses
HERPESVIRUSES

Penyakit HSV-2

1) Genital Herpes

2) Neonatal Herpes

3) Aseptic Meningitis
Herpes Herpes zoster

Herpes simplex virus

Herpes zoster (shingle)

 DNA Enveloped viruses
HERPESVIRUSES

Terapi
 Acyclovir Encephalitis HSV-1
Genital Herpes
Neonatal Herpes HSV-2
 Trifluridine Eye infection HSV-1

 Valacyclovir, Famciclovir Genital Herpes

 DNA Non-enveloped viruses
PAPILOMA VIRUSES
PENYEBARAN
 Skin contact & Genital contact

 Skin warts : pada anak-anak

 Genital Warts : sexually transmitted diseases.

PENYAKIT
 Ada 100 tipe virus papiloma

 Skin – Plantar Warts ( tumor jinak : HPV-1, HPV-4 )

 Genital Warts = Condylomata acuminata ( HPV-6 dan

HPV-11 )
 Carcinoma Uterine, Cervix, Penis, Anus ( HPV-16 dan HPV-18 )

 30 % HPV  genital tract

Human papilloma virus
 DNA Non-enveloped viruses
PAPILOMA VIRUSES

Diagnosa
 Gambaran klinis
 Deteksi antibodi

Terapi
 Genital warts : Tinc. Podophyllin, α- interferron
 Skin warts : Liquid nitrogen , Salicylic acid topically
 Cidofovir : severe HPV infection
 DNA Non-enveloped viruses
PARVOVIRUSES ( B-19 )

Penyakit
 Erythema Infectiosum
 Aplastic Anemia
 Fetal infection ( Kehamilan tmt I – II )  tmt III Janin meninggal.
 Arthritis Erythema Infectiosum
 Chronic B-19 Infection ( FifthDisease )
 Parovirus B19

• Parovirus B19
– ssRNA
– Causes Erythema Infectiosum, also known
as “Fifth Disease” (because it is the fifth
infectious rash after rubeola, rubella,
varicella and roseola)
– “Slapped cheek” appearance, spreading to
trunk and limbs
6. Infeksi Virus pada Sistem Limfatik & Kardiovaskuler

a. Epstein-Barr Virus
b. Cytomegelovirus (CMV)
c. HIV
d. Virus Demam Kuning
e. Virus Dengue
f. Filovirus
g. Virus Marbug
h. Virus Ebola
i. Virus Chikungunya
 DNA Enveloped viruses
A. Epstein-Barr Virus ( EBV )

Penyakit GEJALA
- Microcephalus
 Infectious mononucleosis: - Deafness
 Burkitt’ lymphoma ( Kanker ok virus ) - Jaundice ( ikterus )
 Hairy leukoplakia ( AIDS )
- Pupura
- Hepatospenomegali
 Penularan lewat saliva ( Kissing )

 Infeksi dimulai “ oropharyng “  darah  menginfeksi sel limfosit B (

latent di limfosit B )
GEJALA KLINIS
 Demam, Nyeri tenggorokan, Pembesaran kelenjar limfe, Limpa
membesar, Hepatitis, Encephalitis
Epstein-Barr Virus Infections
Epstein-Barr Virus Infections
(Infectious Mononucleosis)

Epstein-Barr Virus ( EBV )

Large facial Burkitt's
Lymphoma ( EBV )

Burkitt's Lymphoma ( EBV )

 DNA Enveloped viruses
B. CYTOMEGALOVIRUS ( CMV )
PENYAKIT
 Pneumonia ( Immunocompromised )

 Kelainan kongenital

 Penularan : Placenta, Menuysui, Saliva, Kontak seksual, Transfusi

GAMBARAN KLINIS
Kelainan kongenital Kelainan pada dewasa
- Microcephalus -Demam. lemah
- Deafness - Pneumonia
- Jaundice ( ikterus ) - Hepatitis
- Pupura - Diarhe lama ( AIDS )
- Hepatospenomegali - Retinitis (AIDS )
- Kebutaan
 DNA Enveloped viruses
CYTOMEGALOVIRUS ( CMV )

Terapi
 Ganciclovir
 CMV Retinitis : - Valganciclovir
- Cidofovir
- Fomivirsen intra-okuler
Ebola Virus Disease
filoviruses
• First appeared in Africa 1976

• “African Hemorrhagic Fever”

– acute,mostly fatal disease
– causes blood vessel “bursting”
– systemic (all organs/tissues)
– humans and nonhuman primates

• Excluding ‘2000 outbreak

– 1,500 cases
– over 1,000 deaths
 The name Ebola
August 26, 1976 in Yambuku, a town in the north of Zaïre. A 44-
year-old school teacher returned from a small hike. His went to the
doctor and because of his high fever they gave him a quinine shot
which is good against malaria.

A week later, he had uncontrolled vomiting, bloody diarrhea,

trouble breathing and then bleeding from his nose, mouth, and
anus.

He died ~14 days after the onset of symptoms.

He started an epidemic that killed 280 of the 313 infected persons

(88%).
 Ebola
The virus kills gorillas
and chimpanzees and
other monkeys. Because it
kills apes in such high
percentage – they are not
likely to be its natural
host.
 2014 OUTBREAK

27 Juli 2014
 TRANSMISSION

• Natural Host: Fruit bats of the Pteropodidae family

(Hypsignathus monstrosus, Epomops franqueti, and

Myonycteris torquata)

• Source of human infection: Blood, secretions,

organs, or other bodily fluids of infected animals,
Bushmeat
(handling of infected chimpanzees, gorillas, fruit bats, monkeys,
forest antelope, and porcupines found ill or dead or in the
rainforest)
Where does Ebola hide?
• 2002- Fruit Bats
• Antibodies against Ebola
• Ebola Gene sequences in
liver and spleen
• Fruit bats do not show any
symptoms
• Best candidate to be the
reservoir
• More research needs to be
done
ENZOOTIC EPIZOOTIC EPIDEMIC
 Ebola Taxonomy

Scientific Classification
Order: Mononegavirales
Family: Filoviridae
Genus: Ebola like viruses
Species: Ebola
Copyrighted
Dr. Fre:derick A. Murphy, D.V.M., Ph.D. 1976.
Subtypes
– Ebola-Zaire, Ebola-Sudan,Ebola-Ivory Coast
• disease in humans
– Ebola-Reston
• disease in nonhuman primates
 Filoviruses
• First Ebola outbreak: 1976 (Zaire, Sudan)
– Hundreds infected
– 70%-90% fatal
• Sporadic outbreaks still occur in Africa
• Three viruses
– Ebola Zaire
– Ebola Sudan
– Ebola Reston (Virginia)
– Reston, Virginia outbreak
• Occurred in a monkey quarantine facility (JRH Biosciences)
• Monkeys imported from Philippines began dying from HF
• Facility was secured by Army
• Nonpathogenic in humans
 Bats are reservoirs?
– Suspected Ebola virus hosts
• Epomops franqueti (Franquet's epauleted bat)
• Hypsignathus monstrosus (hammer-headed bat)
• Myonycteris torquata (little collared fruit bat)
– Suspectecte Marburg virus host
• Rousettus aegyptiacus (Egyptian fruit bat)
 Case History
Virus and
Source of primary #Case CFR
date of Epicenter(s) Factors contributing to spread
infection s (%)
onset
Marburgvir
us
Marburg and Imported monkeys Dissection of monkeys to harvest
1967 32 22
Frankfurt, Germany; from Uganda organs, nosocomial transmission
Rhodesia (present
1975 Zimbabwe)/South Unknown Nosocomial transmission 3 33
Africa
Kisumu and Nairobi, Exposure in cave?
1980 Nosocomial transmission 2 50
Kenya Monkey contact?

1987 Mombasa, Kenya Exposure in cave? – 1 100

Exposure in gold Repeated primary introductions into

1998 Durba, DRC 154 83
mine humans
Nosocomial and community-based
2004 Uíge, Angola Unknown 252 90
transmission
Presumed primary introductions in 2
Exposure in gold
2007 Kamwenge, Uganda cases, with subsequent person–person 4 25
mine?
Ebola Reston excluded spread
 Virus and Source of primary CFR
Epicenter(s) Factors contributing to spread #Cases
date of onset infection (%)

Zaire
ebolavirus

1976
Case History
Yambuku, Zaire
Unknown Nosocomial transmission 318 88
(present DRC)

1977 Tandala, Zaire Unknown – 1 100

Ogooué-Ivindo Traditional healing practices, nosocomial and

1994 Unknown 49 59
Province, Gabon community-based transmission

1995 Kikwit, DRC Unknown Nosocomial transmission 315 81

Ogooué-Ivindo Consumption of dead

1996 Secondary spread to caregivers 31 68
Province, Gabon chimp
Ogooué-Ivindo Exposure while hunting, traditional healing
1996 Unknown 60 75
Province, Gabon practices
Johannesburg, South Imported from Gabon by
1996 Nosocomial transmission 2 50
Africa infected doctor

Ogooué-Ivindo Hunting and consumption Exposure while hunting, secondary spread to

2001 124 78
Province, Gabon of nonhuman primates caregivers, traditional healing practices

Cuvette Ouest Region, Hunting and consumption Exposure while hunting, secondary spread to
2002 143 89
ROC of nonhuman primates caregivers

Cuvette Ouest Region, Hunting and consumption Exposure while hunting, secondary spread to
2003 35 83
ROC of nonhuman primates caregivers

Kasai Occidental
2007 Unknown Unknown 264 71
Province, DRC
Ebola Reston excluded
Virus and
Source of primary #Case CFR
date of Epicenter(s) Factors contributing to spread
infection s (%)
onset
Sudan
ebolavirus

1976
Case History
Maridi and Nzara,
Sudan
Unknown Nosocomial transmission 284 53

1979 Nzara, Sudan Unknown Nosocomial transmission 34 65

Nosocomial and community

2000 Gulu, Uganda Unknown 425 53
transmission

2004 Yambio, Sudan Unknown Unknown 17 41

Ivory Coast
ebolavirus
Taï Forest, Côte Necropsy of
1994 – 1 0
d’Ivoire chimpanzee
Ebolavirus,
un-known
species
Bundibugyo District,
2007 Unknown Unknown 149 25
Uganda
Ebola Reston excluded
 Virus Ebola
 WHO (9 Agustus 2014):
1848 kasus tercatat  1030 meninggal
Laporan : dalam 3 hari  52 korban meninggal
 Seorang Pastor (Spanyol) 75 tahun.
tertular ebola saat berada di RS Saint Joseph,
Liberia, membantu pengobatan pasien ebola
di RS  Meninggal
CURRENT SITUATION
• Total Cases CDC Updated: August 19, 2014
• Suspected and Confirmed Case Count: 2240
• Suspected Case Deaths: 1229 (61,74%)
• Laboratory Confirmed Cases: 1383
• WHO  18 Aug 2014 Total confirmed, probable, and suspect cases and deaths
from Ebola virus disease : Cases: 2473, Deaths: 1350 (54,59%).
 Ebola Pathogenesis
• Enters Bloodstream
– skin, membranes,open wounds

• Cell Level
– docks with cell membrane

• Viral RNA
– released into cytoplasm
– production new viral proteins/ genetic material

Copyright: Russell Kightley Media, Australia • New viral genomes

– rapidly coated in protein
– create cores
Virus Ebola
 Pathogenesis
• Major clinical feature is inflammatory response resembling septic shock
• Nonhuman primate models show initial replication in
– Monocytes
– Macrophages
– Dendritic cells (blocking maturation to APC)
• Some of these cells disseminate virus throughout the body
• A systemic cytokine and chemokine inflammatory response occurs
• Multisystem organ failure
– Cell surface tissue factor triggers extrinsic coagulation pathway
– Disseminated intravascular coagulation occurs
– Endothelial cell infection appears late in disease
• Two viral proteins suppress the type I interferon response
– VP35 protein inhibits activation of interferon regulatory factor 3
– VP24 blocks STAT1 localization to the nucleus
• Lymphocytes die by apoptosis (and not viral infection)
 Cara Virus Ebola Menyerang Tubuh
1 Virus masuk ke dalam tubuh lewat kontak darah terinfeksi, urin, faeces,
muntahan, sperma, cairan tubuh lain ( Inkubasi 2-21 hari)

2 Virus menyerang sistem imun (kerusakan lekosit)

3 Sel yang terinfeksi virus membawa virus ke seluruh tubuh

4 Membentuk gumpalan darah yang menyebabkan kerusakan organ

 Cara Virus Ebola Menyerang Tubuh
5
Terjadi “cytokine storm”  kerusakan organ

6 Organ yang terkena : Otak, liver, ginjal, usus, mata dan urogenital

Kerusakan sistem vaskuler, perdarahan

7

8 Syok hipovelemik, kehilangan 20% darah, gagal organ

 Virus Ebola

WHO : Virus Ebola tidak ditularkan lewat udara

Incubation Period:
1. Symptoms may appear anywhere from 2 to 21 days after exposure to Ebola, but
the average is 8 to 10 days.
2. Recovery from Ebola depends on good supportive clinical care and the patient’s
immune response.
3. People who recover from Ebola infection develop antibodies that last for at least
10 years.

Symptoms of Ebola :
1. Acute Fever ( > 38.6°C )
2. Severe headache
3. Muscle pain
4. Weakness (malaise)
5. Chest pain (accompanied by cough)
6. Diarrhea (often severe)
7. Nausea - Vomiting
8. Abdominal (stomach) pain
9. Unexplained hemorrhage (bleeding or bruising)
:
Symptoms of Ebola :

1. Maculopapuler rash appears around day 5-7.

2. Edema of the face, neck and/or scrotum
3. Hepatomegali
4. Flushing
5. Conjunctival injection
6. Pharyngitis
7. Around 10-12 days after the onzet 

Improvement Secondary bacterial infection

 Ebola
Symptoms
Symptoms (Days 1-10)
• Replication period
• Inside the body’s
monocytes,
macrophages, and
dendritic cells
• No visible symptoms, but
contagious
Days 11-14
• Body recognizes infection Days 15-19
and responds • Virus attacks connective tissue
• fever, headache, muscle • Blood pools under skin
pain, conjunctivitis, and • Nausea, blood in vomit and diarrhea, and
abdominal pain hemorrhaging from the mouth, nose, and other body
• Virus attaches to blood openings
vessel walls • Hypovolemic shock causing death
• No FDA-approved vaccine
or medicine (e.g., antiviral drug) is available
forEbola.
• Symptoms of Ebola are treated as they
appear. The following basic interventions,
when used early, can significantly improve
the chances of survival:
• Providing intravenous fluids
(IV)and balancing electrolytes (body salts)
• Maintaining oxygen status and blood
pressure
• Treating other infections if they occur
• Experimental vaccines and treatments for
Ebola are under development, but they have
not yet been fully tested for safety or
effectiveness.
• Recovery from Ebola depends on good
supportive care and the patient’s immune
response. People who recover from Ebola
infection develop antibodies that last for at
least 10 years, possibly longer. It isn't known
if people who recover are immune for life or
if they can become infected with a different
species of Ebola. Some people who have
recovered from Ebola have developed long-
term complications, such as joint and vision
problems.
 Diagnosis
• Complicated by non-specific early symptoms
• BSL-3 lab required (BSL-4 for virus isolation)
Timeline of infection Diagnostic tests available
Within a few days after onset  Antigen-capture enzyme-linked
immunosorbent assay (ELISA) testing
 IgM ELISA
 Polymerase chain reaction (PCR)
 Virus isolation

Later in disease course or after  Serology: IgM and IgG

recovery
Retrospectively in deceased patients  Immunohistochemistry testing
 PCR
 Virus isolation
 Treatment

• No Standard Treatment available

• Patients receive supportive therapy
• treating complicating infections
• balancing patient’s fluids and electrolytes
• maintaining oxygen status and blood
pressure
 7. Infeksi Virus Penyebab Tumor

NAMA VIRUS JENIS JENIS TUMOR/KANKER

VIRUS
Hepatitis B Virus DNA Kanker hati

Hepatitis C Virus DNA Kanker hati

Human Papilomavirus Virus DNA Kanker servik, vagina, vulva, orofaring,

(HPV) tipe 16,18 anus , penis
Epstein-Barr virus Virus DNA Limfoma Burkit, Limfoma Non-Hodgkin,
Hodgkin, Kanker nasofaring
Herpes virus 8 Virus DNA Sarkoma Kaposi, castleman’s Disease

Virus Polyoma manusia Virus DNA Limfoma Hodgkin, Kanker kulit, prostat

Humann T-cell Virus RNA Acute T-cell leukemia

lymphotropic virus-1
(HTLV-1)
Virus heapatitis B, C  kanker hati
 Human Papiloma virus tipe 16, 18

• Kanker servik, vagina  Kanker nasofaring

 DNA Enveloped viruses
HUMAN HERPES VIRUS 8

KAPOSI’S SARKOMA
Molluscum contagiosum virus
 Obat antiviral

Virus Saluran Virus pada Hati Virus HIV Virus Herpes &
nafas - Zidovudin CMV
- Adefovir - Stavudin
- Amantadin - Entekavir - Lamivudin - Asiklovir
- Oseltamivir - Interferron - Efapirens - Sidofovir
- Ribavirin - Lamivudin - Tenofovir - Famsiklovir
- Rimantadin - Abakavir - Formivirsen
- Zanamivir - Amprenavir - Forkamet
- Atazanavir - Gansiklovir
- Delavirdin - Pensikovir
- Didanosin - Valasiklovir
- Indinavir - Valgansiklovi
- Ritonavir r
- Indinavir - Viradabin
Replication cycle of an influenza virus