INFEKSI VIRUS

S I LV A N I P E R M ATA S A R I , M . B I O M E D
KARAKTERISTIK VIRUS

• Ukuran kecil 10-300 nm

• Genom : DNA atau RNA
• Metabolisme tidak terjadi di luar sel
• Tidak tumbuh pada media tetapi sel hidup
STRUKTUR
 PROTEIN Coat (kapsid) : - proteksi genom
- anti genic
 Virion : partikel virus
 Kapsomer : unit structural protein
 Asam nukleat
 Envelop : terdiri dari lipoprotein

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CULTIVATION OF VIRUSES

Viruses can only replicate within living cells.

For culture in vitro, 3 main systems are used:
1. Tissue culture: sel diambil dari jaringan manusia/ hewan
dibiakkan dalam media buatan dalam tabung. Sel-sel ini
hidup & mengadakan metabolisme, shg. dapat
menunjang replikasi virus.
2. Chick embryo: beberapa virus dapat ditumbuhkan pada
sel embryo ayam.
3. Laboratory animals: sebelum ada cara lain, virus diisolasi
dan diinokulasi pada hewan coba, seperti tikus, kelinci,
kera.
 DEFINISI

• Infeksi virus  masuknya virus ke dalamtubuh

inang melalui siklus lisis dan lisogenik hingga
timbul gejala sakit.
• Infeksi akut infeksi jangka waktu cepat tapi
fatal
• Infeksi kronis infeksi berkepanjangan sehingga
ada resiko gejala penyakit muncul kembali
 PRINSIP-PRINSIP INFEKSI VIRUS

• Respon seluler terhadap infeksi virus  apoptosis,

nekrosis, hiperplasia atau kanker.
• Prinsip-prinsip penting menyangkut infeksi virus
adalah sebagai berikut:
1. banyak infeksi virus bersifat subklinis
2. infeksi yang sama dapat disebabkan oleh berbagai
virus
3. virus yang sama dapat menyebabkan berbagai infeksi
4. infeksi yang diakibatkan tidak berhubungan dengan
morfologi virus
5. keluaran pada kasus apapun ditentukan oleh faktor
virus, host, dan dipengaruhi oleh gen masing-masing.
• Patogenesis virus  proses virus menginfeksi
inang
• Patogenesis penyakit  suatu bagian dari
kejadian selama infeksi yang menyebabkan
manifestasi penyakit pada inang.
• Sifat virus patogenik  menginfeksi &
menyebabkan tanda-tanda penyakit pada inang.
Port d’entrée = jalur masuk (kulit atau mukosa ,
lubang tubuh)
EFFECTS OF VIRUSES ON CELLS

1. Death: the infection is lethal; causes a cytopathic effect

(CPE) which kills the cell; e.g. multinucleated giant cells/
syncitia, inclusion bodies.
2. Transformation: the cell is not killed, but is changed
from a normal cell to a malignant or cancerous cell.
3. Latent infection: virus remains within the cell in a
potentially active state, but produces no obvious effects
on the cell’s functions.
4. Haemadsorption: some viruses have haemaglutinin in
their outer coats adheres to erythrocytesagglutination
 PENGARUH FISIK & KIMIA
TERHADAP VIRUS
Panas : inaktif 56 oC 30 menit ; 100 oC bbrp detik
Dingin : stabil pada temperatur rendah, dapat
disimpan di suhu -40 oC sd -70 oC tahunan
inaktif : freezing and thawing
Ultraviolet : inaktivasi virus
Inaktivasi : formaldehid, chlorine, iodine, H2O2
Phenol, kloroform, ether : virus envelop Inaktivasi
envelop  resisten
Desinfektan virus : terbaik adalah larutan hypochlorite &
glutaraldehyde.

korosif Sensitif dan iritatif

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VIRUS DISEASES

Most are mild & the viruses makes a complete recovery;

many are silent in the body without causing any
symptoms, which sometimes cause severe disease in an
unusually susceptible patient. Few viral diseases are
severe with high mortality.

Viruses enter the body through 4 main ways:

 Inhalation: via respiratory tract.
 Ingestion: via gastrointestinal tract.
 Inoculation: through skin abrasions, mucous
membranes (e.g. sexual); transfusion; injections;
transplants; via the bite of an arthropod.
 Congenital: i.e. from mother to fetus.
 ANTI VIRUS

Diseases Antivirus
Herpes simplex Acylorofil, Idoxuridine, Vidarabine

Varicella-zoster Acylorofil, Idoxuridine, Vidarabine

Cytomegalovirus Ganciclovir

AIDS Zidovudine

Respiratory SV Ribavirin

Influenza amantadine

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Acyclovir : non toxic terhadap virus menghambat relplikasi virus (sintesa
DNA)
side effect : rash, gangguan GI, ganguan ginjal
Idoxuridine : menghambat sintesaDNA virus
side effect : depresi BM
Vidarabine : menghambat sintesaDNA virus
side efect : depresi BM
Ganciclovir : side effect – netropenia, trombosito-penia, demam, rash,
TFH abnormal, gangguan fungsi ginjal
Zidovudine : menghambat aktv. enzim “reverse transcriptase” dan
repllikasi
side effect : anemia, depresi BM, netropenia, gangguan ginjal dan hati
Ribavirin : menghambat replikasi asam nukleat
side effect : retikulositosis, depresi respirasi
Amantadine : block penetrasi virus terhadap sel
side effect : insomnia, nervousness, lelah
Virus Growth cycle
1. ADSORBSI
a. Adanya reseptor spesifik pd membrane
b. Pada suhu 37 oC, dapat juga 4 oC (slow)
c. Enhanced Mg/Ca
2. ENTRY
a. Invaginasi membrane sel membulat sesuai
partikel Virus
b. Fusi envelop virus dengan membran sel
3. UNCOATING
a. Mengeluarkan genom/asam nukleat
b. Enzim sel – membuka protein coat
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4. TRANSKRIPSI : produksi virus mRNA
Lanjutan
5. SINTESA KOMPONEN VIRUS
Sintesis protein virus : struktural (partikel virus) dan protein non-
struktural (oleh virus polimerase atau replikase)

6. ASSEMBLY
Genom virus akan membentuk partikel virus baru, terjadi pada
inti sel, sitoplasma, membran sel

7. RELEASE
pecahnya atau lisis dari membran sel

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Inge Lusida, Viruses
Mechanisms of budding of enveloped viruses

Inge Lusida, Viruses

 PATOGENESIS VIRUS

1. Proses masuk dan replikasi primer

virus menempel di permukaan kulit, sal. Pernapasan, sal.
Urogenital, atau konjungtiva.
Umumnya virus replikasi di port d’entrée, virus influenza
(pernapasan) dan norovirus (gastrointestinal) menyebabkan
penyakit di port d’entrée dan menyebar lokal dan tidak
sistemik lebih lanjut.
B. Viral Spread & Cell tropism
 Many viruses produce disease at distant from their point
of entry, e.g. enteroviruses.
 Most common route of spread: via bloodstream or
lymphatics. Virus in the blood, called: viremia. The viremic
phase is short in many viral infections.
 Neuronal spread, e.g. in rabies, virus reaches the
brain; in herpes simplex, virus moves to ganglia to initiate
latent infections.
 Tend to exhibit organ & cell specificities; specific cell
surface receptors for that virus.
MEKANISME
PENYEBARAN
VIRUS
MELALUI
TUBUH
PADA
MANUSIA

Inge Lusida, Viruses

C. Cell Injury & Clinical Illness
 Destruction of virus-infected cells in target tissues
 Physiologic alterations by the tissue injury

disease
Some tissues, e.g. intestinal epithelium, can rapidly
regenerate & withstand extensive damage. Differ from
e.g. brain

Clinical Illness:
General symptoms associated with many viral infections (:
malaise, anorexia), result from host response (: such as
cytokine production) or by direct killing the cells.
Clin. symptoms is an insensitive indicator.
Inge Lusida, Viruses
D. Virus Shedding
 Shedding usually occurs from the body surfaces involved
in viral entry.
 Occurs at different stages of disease, depending of
particular virus, at which time the host is infectious.

E. Outcome of Viral Infection

1. Recovery
 virus infections are usually self-limiting
 associated with viral clearance
 host factors influencing
2. Persistence: Chronic & Latent Virus Infections
 VIRUS DISEASE
Invasif : penyebaran keberbagai organ & Jar.
CPE lesi dan disfungsi
Respon hospes thd inf. Virus
Non spesifik : kulit utuh
sal. Nafas : mucus dr epitel
sal cerna : asam lambung
bile-lisis envelop virus
sal kencing
conjunctiva : air mata
fagositosis
Spesifik : humoral eliminasi virus
selular eliminasi sel diinfeksikan virus

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 RESPON SPESIFIK INFEKSI VIRUS

• Humoral  antibodi imunoglobulin:

- dihasilkan sel plasma
- struktur Y shape
- eliminasi virus
Contoh: igA melindungi dari virus yang masuk
melalui pernapasan dan pencernaan.
Melindungi dari reinfeksi virus yang sama.

• Seluler  eliminasi sel menginfeksi virus

(limfosit T sitotoksik)

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(2. Persistence: Chronic & Latent Virus Infections)
The virus persists for long periods of time in the host.
Chronic infections: virus can be continuously detected, often at
low levels, mild or no clinical symptoms. e.g. HBV, HCV
Latent infections:
 virus persists in an occult, or cryptic, form most of the time;
 there will be intermittent flare-ups of clinical disease;
 infectious virus can be recovered during flare-ups.
 e.g. HSV, HZV
Inge Lusida, Viruses
INFEKSI
VIRUS
PADA
JANIN
REFERENCES:

1. Brooks GF, Carroll KC, Butel JS, Morse SA, and

Mietzner TA. Jawetz, Melnick, & Adelberg’s Medical
Microbiology 25th ed. 2010. Lange Medical Books.
2. Brooks GF, Carroll KC, Butel JS, Morse SA, and
Mietzner TA. Jawetz, Melnick, & Adelberg’s Medical
Microbiology 25th ed. 2010. Lange Medical Books.
3. Richman DD, Whitley RJ, Hayden FG. Clinical Virology.
2nd ed. 2002. ASM Press, Washington, D.C.
4. Timbury MC. Notes on Medical Virology. 11th ed. 1997.
Churchill Livingstone.

Inge Lusida, Viruses