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7/22/2019 physiology-and-the-growth-of-virus.ppt
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Physiology and the Growth of virus
Dr. A. Aziz Djamal
MSc.DTM&H,sPmk(k)
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What is a VirusA non-cellular micro-organism with contain
genome ( DNA or RNA ) and protein coat ,lipid
or glycoprotein
Virus (latin) mean Poison/ toxin
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Viral Growth ?
Is it true?Actually Growth-increase in size
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History
1901
FROSCH and LOFFLER- Foot and Mouth DiseaseIWANOSKY Tobacco mozaic virus
Ultrafiltrable agent
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Characteristic
1. No Cellular organel for metabolism.
esp. Ribosome.
2. No growth and no energy yieldingmechanism.
3. Obligate Intracellular.
4. Resistant to antibiotics.5. CMI play more in immunity.
6. Size relatively very small – nanometer
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Method of reproduction
1. No living activities outside living cells.
2. Choose the appropriate cell depend on
specific receptor. A Species virus choosespecific target cell.
3. Process of entering the target cell :
Adsorbtion/attchment, Penetration,
Uncoating, Transcription-Replication,
Synthesis of Viral components, Assembly,
New viral particles, Host cell burst/Budding.
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Viral Classification
Depend much on the kind of cell as target of
any virus :
1. Animal Virus , Include human virus.2. Plant Virus.
3. Bacterial Virus ( Bacteriophage).
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Viral Morphology
Symetry
Eicosa hedral
Hellical
Special type
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Further Classification
Many ways:
1. The way of transmission : Arbovirus
2. Size and genome : Picorna virus.
3. Target organ : Hepatitis virus.
Etc.
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What happen in the target cell
1. Cell death- Cellular burst – CPE.
2. Un-assembly protein – Inclusion body :
Negri bodyPaschen Body.
3. Integration/Insertion of viral genome to
genome host cell—Cellular genetic andphenotypic change—
hyperplasia/Oncogenic development.
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Thank you
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Immunity to viruses
dr erly SpMK
Viruses
- Obligatory intracellular m.o
- replicate within cells
- often using the NA&protein of the
host
- utilizing normal cell surface molecules
as receptors to enter the cell.
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Surface proteins as receptors :
1. CD4 molecule on T cells
2. CR2,CD21 on B cells3. ICAM-1 , CD 54 variety of cell types
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Innate Immunity to Viruses
1. Production IFN-1 by infected cellsinhibit
viral replication2. NK cells lyse infected cells
IFN-1 enhance NK cells to lyse infected
cells
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•Interferon(IFN)
• Glikcoprotein
• Alpha,Betha and Gamma IFN
• Are produced within a few hours of the initiation
of viral replication.• Antibody positive in blood several days after
• Double stranded RNA viruses the most potent
inducers of IFN
• Act by binding to a receptor on the cell surface
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• Do not enter the cell
• No effect to the extracellular viruses
• Alpha and betha IFN
stronger antiviralaction
• Activates macrophages
• Human IFN for human therapy
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NK Cells
• Lymphocyte
• Destroy cells infected by viruses(secreting
perforins & granzymes.
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3. Phgocytosis by macrophage
4. Clearance of mucus by the cilia of perpiratory
tract also important defences
- Increased corticosteroid levelssuppress host
defences and predispose to severe viral infection.
- Malnutrition predispose measles
- Very young&very old have more severe viral
infections
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Spesific Immune Responces to viruses
• A combination of humoral&cellular immune
mechanisms.
• Spesific antibodiesdefence againts viruses
early of infection
defence againts cytopathic viruses
• Netralizing antibodiesprevent viral
attachment&entry into host cells
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• Opsonizing Antibodiesenhance phagocytic
• Secretory IgA netralizing viruses enter
respiratory & intestinal tract
• Antibodies effective againts viruses before
enter cells & block spread from cell to cell.
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Evasion of Immune Mechanism by
Viruses
1. Many viruse are capable of great antigenic
variation.
2. Some viruses inhibit class I MHC
3. Some viruses produce molecules that inhibit
innate or spesific immunity
4. Viruses may infect & either lyse or
inactivate,immunocompetent cells
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Virus DNA
Hepatitis virus
Herpes virus
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Characteristic Hepatitis Virus
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Hepatitis virus
• Produce acute inflammation of the liver
– In Chronic active hepatitis :
Histologic change from inflammation and necrosis
to collaps of the normal reticulum framework with
bridging between the portal triads or terminal
hepatic vein
• Resulting in a clinical illness – Fever
– Gastrointestinal symptoms: nausea, vomite
– Jaundice
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Hepatitis B
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Replication of hepatitis B virus
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Virus Hep-B
• HBV establishes chronic infection
• Major factor in the evantual development of
liver disease and hepatocelluler carcinoma• Transmission modes and response to
infection is vary
▫
Depending on the age at time of infection▫ Infant: during infancy,from infected household
contact chronic
▫ High-risk group
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High-risk group infected by HBV
• Parenteral drug abusers
• Health care personnel
• Multiply trasfused patients• Organ transplant patients
• Hemodialysis patient and staff
• Newborn infant to mother with Hep-B• etc
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HBV
• HBsAg can be detect:
– Saliva, nasopharyngeal washing, semen, mestrual
fluid, vagina secretion, blood
• How HBV transmit to other person?
• HBeAg + in carrier person assumed all the
body fluids is infectious
• Precaution: vaccination
• Laboratory feature:
– Interpretation of HBV serologic markers
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Clinical and serologic event HBV
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Herpes Viruses
• Ability :
– establish lifelong persistent infections in their host
– To undergo periodic reaction
• Frequent reactivation:
– in immunosupressed patients cause serious
health complications
– May be clinically quite different from the primaryinfection
• A large virus
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Herpes simpleks virus
• Extremely widespread in human population
– Broad host range
– Able to replicate in many types of cells
– Grow rapidly and highly cytolytic
– Common recurrences
• Two distinct HSV:
– HSV type 1 spread by contact (often saliva)
– HSV type 2 transmitted sexually or maternal
genital infection to a newborn
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HSV…
• HSV-1 : site latency at trigeminal ganglia
• HSV-2: site latency at sacral ganglia
• How the virus enconter the host?
▫ Mucosal surface or broken skin
• the clinical finding for HSV infection
▫ Oropharyangeal infection
▫ Keratokonjunctivitis
▫ Genital herpes
▫ Skin infection
▫ Encepalitis
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Laboratory finding
• Stain (giemsa stain)
– Scraping base of vesiclemultinucleated giant
cell
• PCR
• serology
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Varisella zozter virus
• Highly contagious disease, chiefly of children
• Characterized clinically:
– Generalized vesicular eruption of the skin and
mucous membranes
– A rash limited in distribution to the skin
innervated by a single sensory ganglion
• may be severe in adult andimmunocompromised children
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Pathogenesis
varisella:
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Varisella zozter virus
• Acute skin lesion
– Also acute inflammation of the sensory nerves
and ganglia
– Induce vesicle formation
– Often only single ganglion may be involved
• Distribution skin lesion corresponds closely to
the areas of innervation from an individual
dorsal root ganglion
• It is not clear what trigger reactivation of
latent varisella-zozter virus in ganglia
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Varisella-zozter virus symptom
• Varisella: – malaise, fever, rash start from trunk,then face,
limb, buccal, paryngeal mucosa
– In 5 days: develop hundreds skin lesion• Zozter
– Start with severe pain in the area of skin or
mucosa – Few days after: vesicle appears over the skin
supplied by the affected nerves
– Complication: post herpetic neuralgia
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Laboratory finding
• Tzanck smear:
– Scraping or swab based of vesicle
• Rapid diagnostic prosedure:
– Viral DNA/virus specifis antigen in vesicle fluid,
skin scraping, or biopsy material
• Cell culture
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Therapy and prevention
• The efectivity of antiviral:
– For immunosuppresed patients, halt progression
• The prevention: vaccin
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Cyto Megalo Virus (CMV)
• Largest genetic content in herpesvirus
• Very spesies-spesific and cell type-specific
– Replicate in vitro inhuman fibroblast
• Infect intrauterincongenital anomalies
• Most CMV infection is in subclinical
– Clinical: An infectious mononucleosis-like
syndrome cell enlarged
– Severe infection in immunosuppressed
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patology
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CMV
• How virus transmission
• Laboratory diagnosis?
• What are the treatments?
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Bahan Ajar PowerPoint®
untuk Bio log i SMA Kelas X Semester Genap
From Biology
by Neil A Campbell, Reece, and M itchell
Di Susun oleh Sugeng Riyanto, S.Pd
V I R U S
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Perbandingan ukuran
Virus (berwarna hijau)
Sel bakteri
(berwarna biru) Sel Eukariotik
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• Partikel yang bersifat parasit obligat pada
sel/makhluk hidup.
• Aseluler (bukan merupakan sel).
• Berukuran sangat renik.
• Di dalam sel inang virus menunjukkan cirimakhluk hidup, sedangkan di luar sel
menunjukkan ciri bukan makhluk hidup.
Virus merupakan :
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Virus Berselubung
Materi Genetik (DNA / RNA)
Selubung Protein (Kapsid)
Kapsul virus
Reseptor Virus
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Ada beragam bentuk tubuh virus, diantaranya :
Batang
Seperti huruf T
Bulat
Polihidris
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• Bertujuan untuk memperbanyak partikel virus.
Replikasi virus terjadi hanya bila virus berada di dalam sel makhlukhidup. Secara umum replikasi terjadi melalui 5 tahapan, yaitu :
1. Absorpsi
2. Penetrasi
3. Sintesis
4. Pematangan / Perakitan
5. Lisis
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Didasarkan pada jenis sel inang yang diserang, virus
diklasifikasikan menjadi 4 kelompok :
1. Virus Penyerang Bakteri / Bakteriofage
2. Virus Protista
3. Virus Tumbuhan
4. Virus Hewan / Manusia
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VIRUS RNA
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Virus H5N1
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Virus H5N1
(Flu burung)
- pengenalan virus H5N1
- penyebab
- gejala
- struktur genetik
- cara penularan
- penanganan pemerintah- pengobatan
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VIRUS R bi
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VIRUS Rabies
Rabies → anjing gila↓
Penykt inf akut pd ssp
↓ virus rabies
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Penyebab :
Adapun vektor dalam penularan
penyakit ini adalah anjing,
kucing dan binatang-binatang
liar seperti kera, kelelawar,rakun, serta rubah.
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Cara Penularan Rabies:
Virus rabies ditemukan dalam jumlah
banyak pada air liur hewan yang
menderita rabies. Virus ini akan
ditularkan ke hewan lain atau ke manusiaterutama melalui :
- Lukagigitan
- Jilatan pada luka / kulit yang tidak utuh
- Jilatan pada selaput mukosa yang utuh- Menghirup udara yang tercemar virus
rabies (jrg terjd)
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Masa Inkubasi:
Masa inkubasi adalah waktu
antara penggigitan sampaitimbulnya gejala penyakit .
Masa inkubasi penyakit rabiespada anjing dan kucing kuranglebih 2 minggu (10 – 14 hr).
Pada manusia 2-3 mgg danpaling lama 1 thn.
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Masa inkbs tgtg :
- Lokasi gigitan, biasanya paling pendek
pd org yg d igigit di kepala, tempat yg
tertutup celana pendek- Bila gigitan tdpt di banyak tempat
- Umur
- Virulensi (banyaknya virus yang masuk
melalui gigitan / jilatan)
Rabies Bentuk Diam :
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- Air liur menetes berlebihan- rahang bwh tdk dpt dikatupkan
- hewan tdk dpt mengunyah dan
menelan makanan
- Tdk ada ingin menyerang atau
menggigit pd hwn
- tubuh mengalami kelumpuhan
- Hewan akan mati dalam bbrp jam
Rabies Bentuk Ganas
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- Hewan agresif dan tdk kenalpemiliknya
- Menyerang org, hwn, dan benda
yang bergrk
- Bila berdiri sikapnya kaku, ekor
dilipat diantara kedua paha blk nya
- Pada anak anjing akan menjd lebih
lincah dan suka bermain , ttp akanmgggt bila dipgng dan akan mjd
ganas dlm bbrp jam
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TANDA RABIES PADA KUCING
– Menyembunyikan diri.
- Banyak mengeong.
- Mencakar-cakar lantai.
- Menjadi agresif.- 2 – 4 hr stlh gejala pertama biasa
terjd kelumpuhan, terutama di
bagian belakang.
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Gejala Rabies Pada Manusia :
- demam rgn /sdg, skt kpl, nafsu mkn↓
- lemah, mual, muntah dan terasa ab
normal pd sekitar ggtan (rasa pns,nyeri berdenyut)
- Rasa takut yg sgt pd air, dan peka
terhdp chy, udara, dan suara
- Air liur dan air mata keluar >
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- Pupil mata membesar
- Bicara tidak karuan
- selalu ingin bergrk
- nampak kesakitan
- kejang lalu- lumpuh
- akhirnya meninggal dunia
B t k A t ti
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Bentuk Asystomatis.
- Hewan tidak ada gejala skt.
- Hewan tiba-tiba mati
Patofisiologi
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Vir rabies (liur hwn ter inf)
↓ gigitan / jilatan pd
kulit yg tdk utuh
mns hwn
↓
saraf
medula spinalis otak
↓
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kembangbiak
dgn kecpt 3mm / jam.↓
virus pindah lg
mel saraf ↓
kelj. Ludah
↓ air ludah
Pada 20% penderita, rabies dimulai dengan :
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Pada 20% penderita, rabies dimulai dengan :
kelumpuhan pada tungkai bawah yangmenjalar ke seluruh tubuh. Tetapi penyakit ini
biasanya dimulai dengan periode yang pendek
dari depresi mental, keresahan, tidak enak
badan dan demam. Keresahan akan meningkat
menjadi kegembiraan yang tak terkendali dan
penderita akan mengeluarkan air liur.
Kejang otot tenggorokan dan pita suara
bisa menyebabkan rasa sakit yang luar
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bisa menyebabkan rasa sakit yang luar
biasa. Kejang ini terjadi akibat adanya
gangguan daerah otak yang mengatur proses menelan dan pernafasan. Angin
sepoi-sepoi dan mencoba untuk minum air
bisa menyebabkan kekejangan ini. Oleh
karena itu penderita rabies tidak dapat
minum, gejala ini disebut hidrofobia (takut
air). Lama-kelamaan akan terjadi
kelumpuhan pada seluruh tubuh, termasuk
pada otot-otot pernafasan sehingga
menyebabkan depresi pernafasan yang
dapat mengakibatkan kematian.
Tahapan Penyakit Rabies
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Perjalanan penyakit rabies pada anjing dan
kucing dibagi dalam 3 fase (tahap).
1. Fase Prodormal :
- hwn mencari tpt dingin dan menyendirittp dpt menjd lbh agresif dan nervus,
- pupil mata melbr & tbh kaku 1-3 hr .
↓
fase Eksitasi atau
lgsng ke fase Paralisa.
2 Fase Eksitasi :
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2. Fase Eksitasi :
- hewan menjd ganas
- menyerang siapa saja yg ada di
sektrnya dan memkn brng yg aneh2
- mata menjd keruh dan terbuka
- tubuh gemetaran
↓
fase paralisa
3 Fase Paralisa :
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3. Fase Paralisa :
- Hewan lumpuh pd slrh tubuh
- berakhir dengan kematian.
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Cara Pencegahan:
Langkah untuk mencegah rabies bisa
diambil sebelum terjangkit virus atau
segera setelah terjangkit. Sebagai
contoh, vaksinasi bisa diberikankapada orang-orang yang beresiko
tinggi terhadap terjangkitnya virus,
yaitu :
Cara Penanganan:
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Penanganan Pertama Terhadap Orang
Yang Digigit (Korban)
1. Sgr cuci luka gigitan dgn air bersih dan
sabun / detergen slm 10 sp 15 mnt
(gigitan yg dlm disemprot dng air
sabun )bilas dng air yg mengalir , lalu
keringkan dgn kain bersih.
2. Luka diberi obat luka (betadin), balut3. bawa ke Puskesmas atau Rumah Sakit
perawatan lebih lanjut.
Penanganan Terhdp Hwn Yg Menggigt:
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- curigai hwn yg menggt dgn rabies- berikan tindakan:
- Tangkap hwn tsb → dinterna- Observasi 14 hr
- Hsl obs (+) → vaksinasi rabies
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HEMATOSEROLOGI INFEKSI VIRUS
Prof. dr.RISMAWATI YASWIR, SpPK(K)
HEMATOSEROLOGI INFEKSI VIRUS
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1 ANAMNESA
2PEMERIKSAAN FISIK
3PEMERIKSAAN PENUNJANG
• LABORATIRIUM
• RADIOLOGI
PEMERIKSAAN LABORATORIUM UNTUK
INFEKSI VIRUS
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INFEKSI VIRUS
1
PEMERIKSAANHEMATOLOGI
2
PEMERIKSAAAN
SEROLOGI(PEMERIKSAAN
VIROLOGI)
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PENYAKIT INFEKSI VIRUS INI SANGAT BANYAKSEKALI DIANTARANYA:
• Demam Dengue
• Demam Berdarah Dengue
• HIV/AIDS
• Infeksi Mononukleosis Infeksiosa
• Morbili
• Varicella• Hepatitis
• Meningitis Virus
• Chikungunya
PEMERIKSAAN HEMATOLOGISECARA UMUM UNTUK INFEKSI
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VIRUS
PERDARAHAN , DIC
PENINGKATAN HEMATOKRIT, HIPOALBUMINEMIA
TEST TOURNIQUET + (RL +)
TROMBOSITOPENIA
LEUKOPENIA
PEMERIKSAAN VIROLOGIS
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PEMERIKSAAN VIROLOGIS TIDAK BEGITUSERING DILAKUKAN, HAL INI DISEBABKAN:
Virus yang berukuran 0,02-0,3 µM
tidak bisa diperiksa dibawah
mikroskop cahaya baru bisa
dengan mikroskop elektron
Virus lebih sulit dibiak daripada
kuman & virus hanya dapatbereplikasi pada sel host
PEMERIKSAAN VIROLOGIS
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Untuk biakan (invitro)seringdigunakan organ-organ binatang atau
biakan jaringan sebagai medium
karena memerlukan sel hidup
Memerlukan laboratorium khusus
(sarana lengkap)
Dalam praktek sehari-hari sulit
mengenal infeksi virus dibandingkaninfeksi bakteri
TEST SEROLOGI
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• Test IFA• Test ELISA (Ab IgM dan IgG)
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DEMAM
DENGUE
INFEKSI
VIRUS
DENGUE
DEMAM
BERDARAH
DENGUE
DEMAM DENGUE
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KLINIS: Demam, ruam kulit, sembuhsendiri setelah beberapa hari
LABORATORIUMNYA:
• Test Tourniquet +
• Leukopenia
• Trombisitopenia (kadang)
Tingkat kefatalannya rendah
DEMAM BERDARAH DENGUE
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ADA 2 FASE:• FASE I: Penyakit ringan
demam, nausea, muntah,
malaise, sakit kepala,
test tourniquet +
• FASE II: peningkatan Ht
trombositipeniahipoalbuminemia
efusi pleura
shock DSS
DEMAM BERDARAH DENGUE
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PEMERIKSAAN LABORATORIUM• Isolasi virus paling baik
• dibutuhkan virus > dalam darah
waktu pendek
• Pemeriksaan lama
• Peralatan khusus
• Mahal
UJI HAMBATAN HAEMOGLUTINASI(HAEMOGLUTINATION-
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(
INHIBITION)
• Gold standart
• Darah diambil 2x
Akut
Konvalesen (7 hari setelah diambil I)
ada peningkatan titer ≥ 4 infeksi
• Waktu lama
• Variasi antar laboratorium >
PENINGKATAN TITER ANTIBODI DALAM SERUM
ANTI DENGUE IgM DAN IgG
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ANTI DENGUE IgM DAN IgG
• Metode ELISA
waktu lama
mahal
sensitivitas & spesifisitas tinggi
• Rapid Test
banyak sekarang
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PADA FASE AKUT ANTIGEN DIPERIKSADENGAN RT-PCR
DIAGNOSIS:KLINIS + LABORATORIUM
KELAINAN HEMATOLOGI PADA DHF
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a. Hemokonsentrasi (kebocoran vaskuler →
plasma)Ht ≥ 20% dari nilai rujukan normal sesuai umur
b. Leukopenia →→ depresi SST→ netropenia.limfositosis → respon imun spesifik infeksi dengue
c. LPB/limfosit atipik
respon imun spesifik dengue thdp sel limfosit
proliferasi dan transformasi, sel besar, RNA >>
(Romanowsky : sitoplasma biru)
• Hari 3-8 puncak hari 6
• LBP ≥ 15% limfosit atau ≥ 4% leukosit
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d. Trombositopeni < 100.000/uL• Komplek virus-antibodi permukaan trombosit
agregasi
• Depresi sumsum tulang hiposeluler
megakariosit (hari ke 4)
• Perdarahan, DIC Trombosit
PEMERIKSAAN HEMATOLOGI
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TEST TOURNIQUET
TROMBOSIT
SEDIAAN HAPUS DARAH TEPI
DEMAMBERDARAH
DENGUE
Pem Leukosit
Hematokrit
1. TEST TOURNIQUET
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TUJUAN: Menguji ketahanan kapiler darah
ALAT: tensimeter
stopwatch
PENILAIAN: Petechie
> 10 (+)
2. TROMBOSIT
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NORMAL: 150.000- 400.000/mm3
ALAT: Mikroskop
Hemocytometer
Kapas Alkohol
Lanset
PENILAIAN: < 150.000/mm3 Trombositopenia
> 400.000/ mm3 Trombositosis
3. SEDIAAN HAPUS DARAH TEPI
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DITEMUI BANYAK LIMFOSIT PLASMA BIRU (LPB)
HIV / AIDSVi HIV 1 d HIV 2 HIV
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Virus HIV-1 dan HIV-2 HIV
Menyerang sel limfosit T CD4+ bereplikasi
lisis sel TCD4+ ↓↓ dalam darah
Virus HIV virus RNA untai ganda
famili retrovirus genus lentivirus
Sifat sitopatik merusak sel
Target
menginfeksi sel sistim imun limfosit T CD4 + (Th), makrofag, sel dendrit
Masuk sel menembus membran sel T CD4+ melaluigp120 dan gp41
Gambar Struktur Virus HIV - 1
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INFEKSI HIV DAPAT DI BAGI3 FASE :
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1.Fase Akut (early infection)- Infeksi sel T CD4+ memori
jaringan limfoid mukosa
- Kematian sel-sel terinfeksi dalam
2 minggu infeksi
sel T CD4+ >> dihancurkan
(mukosamemori T CD4+ dalam 4 hari
terinfeksi ± 60%, dlm 1 minggu
80%)
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2. Transisi dari fase akut ke fase kronik- penyebaran virus, viremia
- terbentuk imun respon di “Host”
untuk kontrol sebagian infeksi danproduksi
virus (± 12 minggu setelah infeksi)
3. Fase kronik dari penyakit- kelenjar limfe dan limpa sebagai tempat
replikasi virus HIV destruksi sel ↑↑
T CD 4 + < 200 sel/uL
Gambar Progresifitas infeksi HIV
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Abbas 2007
Kelainan Hematologi pada HIV / AIDS
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• Sel T CD4+ me- oleh karena : – Viral budding terinfeksi efek sitopatik HIV
apoptosis
– Pembentukan syncytium sel multinuclear besar
Umur sel T CD4+ < N – Gangguan fungsi sel T CD4+ :
• aktivasi makrofag
• induksi sel T CD8, sel B, sel NK
• Sel B terinfeksi HIV pengaktifan abnormal
hipergamaglobulinemia poliklonal IgG dan IgA
pe- regulasi sel T CD8+ terhadap sel B
unregulated sel B
Kelainan Hematologi pada HIV /AIDS
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• Monosit dan makrofag yang terinfeksi HIV : – Dapat berikatan dengan envelope HIV ok
mempunyai reseptor permukaan CD4
– Monosit terinfeksi→
reservoir HIV ok tahantehadap efek sitopatik HIV
– Menghasilkan inhibitor IL-1 :
• proliferasi sel T CD4
• kemampuan fagositosis
Imunodefisiensi
ANEMIA
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• Kelainan paling sering: – Dipengaruhi progresifitas infeksi HIV
– Umumnya terjadi pada HIV stadium
lanjut – Me- bila terjadi infeksi oportunistik
dengan kadar Hb 9,7 – 11,7 g/dL dan Ht
36%
Penyebab anemia :
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a. Gangguan produksi eritrosit di SST:
- Anemia penyakit kronis
dgn Fe serum ; TIBC; feritin
- Infeksi HIV dilepas berbagai sitokin
TNF,
IL-1, INF respon eritropoietin di
SST
produksi eritropoietin
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b. Destruksi eritrosit ↑↑ ok proses hemolisis- Autoimun ok dihasilkan autoantibodi oleh sel B
unregulated
- Non Imun : obat utk terapi HIV & infeksi oportunistik yg
bersifat oksidator
anemia hemolitik pada HIV dengan defisiensi enzim G6PD
c. Efek Infeksi Parvovirus B19
Parvovirus menginfeksi prekursor eritrosit hipoplasia
eritroid PRCA
d. Efek obat untuk infeksi HIV
Zidofudin bersifat antimetabolit
LEUKOPENIA
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• Pada infeksi awal, asimptomatik 10%Pada imunodefisiensi lanjut 50% penderita
• Kelainan jumlah dan fungsi leukosit
Limfosit, netrofil, monosit gangguan
imunitas seluler dan humoral
• Netropeni bersamaan anemia
autoimun
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• Me- pertumbuhan koloni dari progenitor sel CFU-GM granulosit dan monosit
Obat infeksi HIV antimetabolit danimunosupresif (ganciclovir)
• Antibodi antinetrofil → me- jumlahnetrofil dan gangguan fungsi kemotaksis,
bakterisidal dan fagositosis
TROMBOSITOPENIA
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• Terjadi karena : – Pe- destruksi trombosit ok antibodi
terhadap antigen trombosit HIV – ITP
– Pe- produksi trombosit di SST
KELAINAN HEMOSTASIS PADA INFEKSI HIV
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Didapat antikoagulan lupus dan ACA→ infeksi oportunistik
DIAGNOSISLABORATORIUM HIV
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• Awal, antibodi (-) – Biakan virus→ waktu 4 minggu
– Deteksi antigen→ ELISA→ protein p24
– Deteksi materi genetik dalam darah
• Deteksi antibodi→ pemeriksaan serologi
komponen virion HIV
Untuk menentukan saat dimulai pengobatan :
- Jumlah limfosit T CD4+
- Jumlah virus HIV (viral load)
INFEKSI MONONUKLEOSISINFEKSIOSA
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• Disebabkan infeksi virus, EBV, CMV, HSV,• Terjadinya limfositosis yang diinduksi oleh respon
terhadap agen infeksius
• Di darah tepi limfosit > 50% dengan limfosit reaktif
Bentuk : - plasmasitoid- monositoid 20%
- limfoplasmasitoid
• Limfosit reaktif dari sel T sesuai dengan antibodi seluler
yang terbentuk setelah sembuh
→ limfosit reaktif merupakan manifestasi akhir dari
infeksi, tidak terdeteksi pada infeksi awal
Klinis Mononukleosis Infeksiosa
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1. Demam, faringitis2. Pembesaran kelenjar limfe
Gambaran Laboratorium:Hematologi:
Kelainan leukosit: leukopenia, normal,
leukositosis Dari hitung jenis: Limfositosis relatif
Pemeriksaan Serologi:
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bisa secara ELISA dan RAPID• Pemeriksaan secara ELISA thdp IgM dan IgG
• Pemeriksaan RAPID secara IMFA thdp IgMdan IgG
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CHIKUNGUNYA
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DEMAM VIRAL DISEBABKAN VIRUSDITULARKAN MELALUI GIGITAN NYAMUKSPESIES STEGOMYIA AEGYP
Masa Inkubasi: 2-4 Hari
Penyakit ini mirip DHF
GEJALA KLINIS
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• Demam mendadak sampai 39 C
• Sakit perut, mual, muntah
• nyeri pada persendian terutama sendi lutut,
pergelangan, jari kaki dan tangan serta tulang belakang• Bintik-bintik kemerahan pada kulit
• Sakit kepala
• Infeksi konjungtiva
• Fotofobia
• Biasa berlangsung 7 hari sembuh sendiri
LABORATORIUM
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Test Serologis Chikungunya
Antibodi IgM
1. Metode ELISA
2. Hemaglutinasi inhibisi
ETIOLOGI: Korona Virus
SARS(SEVERE ACUTE RESPIRATORY SYNDROME)
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ETIOLOGI: Korona Virus
MASA INKUBASI: 2-7 Hari
PENYEBARAN: Melalui dropletTitik air diudara
KLINIS: demam, batuk, sesak nafas, sakit
kepala, sakit tenggorokan, berat
penyakit bervariasi, ringan sedang
sampai berat dan dapat fatal.
LABORATORIUM
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• Leukopenia
• Limfopenia
• Trombositipenia
• SGPT (Alanin Transferase) meningkat• Saturasi O2 Arterial kurang (< 95%)
pada 80% kasus
• PCR-RNA bahan: serum, sekresi nasal &
feses
• Isolasi virus dapat dilakukan tetapi sangat
sulit
RADIOLOGI
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INFILTRAT PULMONAL
FLU BURUNG (AVIAN FLU)
PADA MANUSIA
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• ETIOLOGI: Virus H5N1Menyerang unggas
Dari UnggasManusia
• MASA INKUBASI: Unggas 4 Minggu
Manusia 2-4 Hari
• Virus H5N1 Sangat Virulen
GEJALA KLINIS
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NYERI OTO
DIARE, MUNTAH, RHINORRHEA
RADANG MATA, SAKIT LEHER
SESAK NAFAS GAGAL RESPIRASI AKUT
DEMAM TINGGI, TENGGOROKAN MERADANG
• HEMATOLOGI
PEMERIKSAAN LABORATORIUM
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HEMATOLOGI
Jumlah Leukosit bervariasi:Normal,Leukopenia & Leukositosis
Jumlah Limfosit menurun
Jumlah Trombosit sering menurun
• TEST FAAL HATISGPT meningkat (Sedang)
• TEST FAAL GINJALTerganggu sedikit
PEMERIKSAAN LABORATORIUM
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• TEST SEROLOGIEIA (Enzyme Immuno Assay)
IMMUNOFLURESEN
Tes ini dilakukan 2x
Permulaan Penyakit
10-15 hari kemudian
Terjadi peningkatan titer
(minimal 4x pemeriksaan)
PEMERIKSAAN LABORATORIUM
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• BIAKAN VIRUSSpesimen dari swab faring &
cucian aspirasi hidung dan nasofaring
Hasil 72 jam:
Test Hemaglutinasi inhibisi
PCR- RT_PCR
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ERLINA RUSTAM
ANTI VIRUS
Pengembangan obat anti virus untuk
h t b t b l i
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pencegahan atau pengobatan belum mencapai
hasil seperti yang diinginkan , karena obat antivirus yang dapat menghambat atau membunuh
virus juga akan merusak sel hospes dimana virus
itu berada.
Siklus replikasi virus yang di anggap sangat mirip
dengan metabolisme normal manusia
menyebabkan setiap usaha untuk menekanreproduksi virus juga dapat membahayakan sel
yang terinfeksi.
ANTIVIRUS
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VIRUS parasit intrasel yang tidak bisa bereplikasi
sendiri, tetapi harus menggunakan sel inang.
ANTIVIRUS
Sebuah agen yang membunuh virus
dengan menekan kemampuan untuk
replikasi, menghambat kemampuan
untuk menggandakan danmemperbanyak diri
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Ukuran : sangat kecil (20-300 nm)
50 x lebih kecil dari bakteri
Tidak dapat dilihat dengan mikroskop biasa, digunakan mikroskop elektron
Virus hanya mempunyai DNA dan RNA
Mampu meperbanyak diri, tetapi hanya dalam sel hidup (host)
Dalam Host, dapat bersifat mematikan atau inaktif
Menggunakan DNA atau RNA nya sendiri untuk menginstruksikan sel host membuat
salinan2 baru
Virus bukan sel
Komponen virus sangat simpel
Tidak mampu mensintesis protein dan membentuk ATP
173
Virus
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Secara garis besar dapat dibagi menjadi 10 langkah :
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Secara garis besar dapat dibagi menjadi 10 langkah :
1.Absorpsi virus ke sel pengikatan2. Attachment
3. Penetrasi virus ke sel
4. Uncoating ( dekapsidasi )
5. Transkripsi tahap awal
6. Translasi tahap awal
7. Replikasi genom virus
8. Transkripsi tahap akhir9.Assembly virus
10.Penglepasan virus
Klasifikasi Obat Antivirus
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1. Antinonretrovirus Antivirus untuk herpes
Antivirus untuk influenza
Antivirus untuk HBV dan HCV
2. Antiretrovirus
Nucleoside reverse transcriptase inhibitor ( NRTI )
Nucleotide reverse transcriptase inhibitor ( NtRTI )
Non – nucleoside reverse transcriptase inhibitor (NNRTI)
Protease inhibitor (PI)
Viral entry inhibitor
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Nucleoside reverse transcriptase inhibitor (NRTI)
Nucleotide reverse transcriptase inhibitor (NtRTI)
Non- Nucleoside reverse transcriptase inhibitor (NNRTI)
Protease inhibitor (PI) 177
ANTI NONRETROVIRUS
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ANTI NONRETROVIRUS
A.Antivirus untuk herpes
Obat – obat yang aktif terhadap virus herpes
umumnya merupakan antimetabolit yangmengalami bioaktivasi melalui enzim kinase
sel hospes atau virus untuk membentuk
senyawa yang dapat menghambat DNApolimerase virus .
.
1.Asiklovir Mekanisme Kerja
dimetabolisme menjadi asiklovir trifosfat melalui 3
h f f il k h b A
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tahap fosforilase, yang akan menghambat DNA
polimerase virus.
Resistensi
Disebabkan oleh mutasi pada gen timidin kinasevirus atau pada gen DNA polimerase.
Dosis
5 x 200 mg untuk 10 hari -------- untuk HSV3 x 200 mg untuk 1 bulan-------untuk herpes genital
Salep Asiklovir 5% 6 x sehari utk 7 hr ----…..---------
Indikasi
I f k i HSV 1 d HSV 2 b ik l k l i t ik
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Infeksi HSV-1 dan HSV-2 baik lokal maupun sistemik
( termasuk keratitis herpetik , herpetik ensefalitis,herpes genitalia,herpes neonataldan herpes labialis )
dan infeksi VZV ( varisela dan herpes zoster ).
Efek samping
Mual, muntah dan pusing , namunAsiklovir pada
umumnya dapat ditoleransi dengan baik.
Pemberian selama kehamilan tidak dianjurkan
2. VALASIKLOVIR
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Mekanisme Kerja
sama dengan asiklovirResistensi
sama dengan asiklovir
Indikasi
Efekif utk terapi infeksi yang disebabkan oleh HSV, VZV dan
sebagai profilaksis terhadap penyakit yang disebabkan CMV.
Efek samping
sama dengan asiklovir
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23.12.2006
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B. Antivirus Untuk Influenza
Contoh: Amantadin dan Rimantadin
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Mekanisme Kerja
Merupakan antivirus yang bekerja pada protein M2 virus , suatukanal ion transmembran yang diaktivasi oleh pH
Absorbsi saluran cerna baik, tidak dimetabolisme dihati dan
ekskresi dalam bentuk utuh, t ½ 16 jam
Resistensi
Terjadi nya mutasi pada domain transmembran protein M2 virus.
Indikasi
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Indikasi
Pencegahan dan terapi awal infeksi virus influenza A .Juga diindikasikan untuk terapi penyakit parkinson
Dosis: 2 x 100 mg
Efek samping Yang tersering adalah gangguan GI ringan yang tergantung dosis .
Efek samping pada SSP seperti kegelisahan , kesulitan
berkonsentrasi, insomnia, hilang nafsu makan, kejang bahkan koma.
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C. Antivirus untuk HBV dan HCV
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1.Lamivudin
Lamivudin merupakan L-enantiomer analog deoksisitidin .
Lamivudin bekerja dengan cara menghentikan sintesis DNA ,
secara kompetitif menghambat polimerase virus ( reversetranscriptase , RT ) .
Resistensi
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Resistensi
Resistensi terhadap lamivudin disebabkan oleh mutasi padaDNA polimerase virus
Indikasi
Infeksi HBV ( wild –type dan precore variants )
Efek samping
Umumnya dapat ditoleransi dengan baik .
Efek samping yang terjadi : fatigue, sakit kepala dan mual.
2. ADEFOVIR
Mekanisme kerja dan resistensi
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Adefovir merupakan analog nukleotida asiklik. merupakanpenghambat replikasi HBV sangat kuat yang bekerja tidak hanyasebagai DNA chain terminator , namun juga meningkatkanaktivitas sel NK dan menginduksi produksi interferon endogen.
IndikasiEfektif dalam terapi infeksi HBV yang resisten tehadap
lamivudin.
Efek Samping Umumnya adefovir 10 mg /hari dapat ditoleransi dengan baik.
ANTIRETROVIRUS
A. Nucleoside Reverse Transcriptase Inhibitor
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A. Nucleoside Reverse Transcriptase Inhibitor
(NRTI )Antivirus golongan ini bekerja pada tahap awal replikasi HIV ,
dengan menghambat terjadinya infeksi akut sel yang rentan ,
tapi hanya sedikit berefek pada sel yang telah terinfeksi HIV.
Untuk dapat bekerja , semua obat golongan NRTI harus
mengalami fosforilasi oleh enzim sel hospes di sitoplasma
.Karena NRTI tidak memiliki gugus 3`-hidroksil , inkorporasi
NRTI ke DNA akan menghentikan perpanjangan rantai.
1. ZIDOVUDIN
Mekanisme Kerja
Target zidovudin adalah enzim reverse transcriptase ( RT ) HIV.
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Target zidovudin adalah enzim reverse transcriptase ( RT ) HIV.
Bekerja dengan menghambat enzim RT virus , setelah ggsazidotimidin(AZT)pada zidovudin mengalami fosforilasi.
Resistensi
Resistensi disebabkan oleh mutasi pada enzim RT.
IndikasiInfeksi HIV , dalam kombinasi dengan anti HIV lainnya seperti
lamivudin dan abakavir
Efek Samping
Granulositopenia dan Anemia setelah 2-6 minggu terapi
(periksa darah lengkap setelah 1-2 minggu pemakaian)
sakit kepala, mual, insomnia.
2. DIDANOSIN
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Mekanisme KerjaObat ini bekerja pada HIV RT dengan cara menghentikan
pembentukan rantai DNA virus
Resistensi
Disebabkan oleh mutasi pada RT.Indikasi
Infeksi HIV , terutama infeksi HIV tingkat lanjut , dalam
kombinasi dengan anti-HIV lainnya .
Efek samping
Diare, pankreatitis, neuropati perifer.
B. NUCLEOTIDE REVERSE TRANSCRIPTASE
INHIBITOR ( NtRTI )
Tenofovir disoproksil fumarat merupakan NtRTI
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Tenofovir disoproksil fumarat merupakan NtRTI
pertama untuk terapi infeksi HIV -1 .
Obat ini digunakan dalam kombinasi dengan obat
anti retrovirus lainnya.
Tidak seperti NRTI yang harus melalui 3 tahap
fosforilase intraseluler untuk menjadi bentuk aktif ,
NtRTI hanya butuh 2 tahap fosforilasi saja .
Dengan berkurangnya satu tahap fosforilasi , obat
dapat bekerja lebih cepat dan konversinya menjadi
b t k ktif l bih
1. TENOFOVIR DISOPROKSIL
Mekanisme Kerja
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bekerja pada HIV RT ( dan HBV RT ) dengan caramenghentikan pembentukan rantai DNA virus.
Resistensi
Disebabkan oleh mutasi RT kodon 65
Indikasi
Infeksi HIV dalam kombinasi dengan evafirenz , tidak boleh
dikombinasikan dengan lamivudin dan abakavir
Efek Samping
mual, muntah , flatulens , diare
C. NON –NUCLEOSIDE REVERSE
TRANSCRIPTASE INHIBITOR ( NNRTI )
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NNRTI merupakan kelas obat yang menghambat
aktivitas enzim RT dengan cara berikatan di tempat
yang dekat dengan tempat aktif enzim dan
menginduksi perubahan konformasi pada situs aktif
ini.
1. NEVIRAPIN
Mekanisme kerja
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Mekanisme kerja
bekerja pada situs alosterik tempat ikatan non – subtrat HIV -1 RT
Resistensi
resistensi disebabkan oleh mutasi pada RT
Indikasi
infeksi HIV -1 , dalam kombinasi dengan anti-HIV lainnya ,terutama NRTI
Efek Samping
ruam, demam, fatigue, sakit kepala,somnolens, mual, danpeningkatan enzim hati.
2. DELAVIRDIN
Mekanisme kerja
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j
sama dengan nevirapinResistensi
Disebabkan oleh mutasi pada RT
Indikasi
infeksi HIV -1 , dikombinasikan dengan anti HIV lainnya
terutama NRTI
Efek Samping
ruam, peningkatan tes fungsi hati .
Pernah di laporkan menyebabkan neutropenia
D. PROTEASE INHIBITOR ( PI )
Semua PI bekerja dengan cara berikatan secara
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reversibel dengan situs aktif HIV- protease.HIV-protease sangat penting untuk infektifitas virus
dan penglepasan poliprotein virus .Ini menyebabkan
terhambatnya penglepasan polipeptida prekusor
virus oleh enzim protease sehingga menghambatmaturasi virus , maka sel akan menghasilkan partikel
virus yang imatur dan tidak virulen.
Resistensi terhadap PI secara umum berlangsung
lewat akumulasi mutasi gen protease
1. SAKUINAVIR
Mekanisme Kerja
Sakuinavir bekerja pada tahap transisi merupakan
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Sakuinavir bekerja pada tahap transisi , merupakan
HIV protease peptidomimetic inhibitor
Resistensi
Disebabkan oleh mutasi pada enzim protease
.terjadi resistensi silang dengan PI lainnyaIndikasi
infeksi HIV , dalam kombinasi dengan anti HIV lain (
NRTI dan beberapa PI seperti ritonavir )
Efek Samping
Diare, mual, nyeri abdomen .
2. INDINAVIR
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Mekanisme Kerjasama dengan sakuinavir
Indikasi
Infeksi HIV , dalam kombinasi dengan anti HIV lainnyaseperti NRTI
Efek Samping
Mual, hiperbilirubinemia, batu ginjal
E. VIRAL ENTRY INHIBITOR
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Enfuvirtid merupakan obat pertama golongan viralentry inhibitor .
Obat golongan ini bekerja dengan menghambat fusi
virus ke sel. Selain enfurtid bisikla saat ini sedang
dalam study klinis , dimana obat ini bekerja dengan
cara menghambat masukan HIV ke sel melalui
reseptor CXCR4
1.ENFUVIRTID
Mekanisme Kerja
Enfuvirtid menghambat masuknya HIV 1 ke dalam
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Enfuvirtid menghambat masuknya HIV-1 ke dalam
sel dengan cara menghambat fusi virus ke membransel. Enfuvirtid berikatan dengan bagian HR-1 ( firstheptad-reat)pada sub unit gp41 envelopeglikoprotein virus serta menghambat terjadinya
perubahan konformasi yang dibutuhkan untuk fusivirus ke membran sel
Resistensi
perubahan genotip pada gp41 asam amino 36-45menyebabkan resistensi terhadap enfuvirtid
Indikasi
terapi infeksi HIV -1 dalam kombinasi dengan anti -
HIV lainnya.
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Efek Samping
efek samping yang tersering adalah reaksi lokal
seperti nyeri, eritema, pruntus, iritasi, dan nodulatau kista
PENGGUNAAN KLINIS OBAT ANTIVIRUS
Tujuan utama terapi antivirus pada pasien
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imunokompeten adalah menurunkan tingkatkeparahan penyakit dan komplikasinya , serta
menurunkan kecepatan transmisi virus .
Sedangkan pada pasien dengan infeksi virus kronik ,
tujuan terapi antivirus adalah mencegah kerusakan
oleh virus ke organ viseral , terutama hati , paru,
saluran cerna dan sistem saraf pusat.
Beberapa hal yang perlu di pertimbangkan dalam
penggunaan obat antivirus:
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• Lama terapi
• Pemberian terapi tunggal atau kombinasi
• Interaksi obat
• Kemungkinan terjadinya resistensi
Pemilihan obat anti virus
1. Infeksi HIV atau AIDS
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Pengobatan anti-virus pada dasarnya menyerang virus HIV di salah
satu dari dua tempat berikut :
i. menjaga virus tetap berada di luar sel-T yang sehat;
ii. mencegah sel-T yang terinfeksi untuk melepaskan sel virus baru.
Perawatan lain termasuk meningkatkan sistem kekebalan alami,
supaya bisa melawan HIV. Ini disebut 'modulasi kekebalan.
Gejala HIV tidak muncul selama beberapa tahun, karena sistemkekebalan alami tubuh melawan HIV. Obat-obat anti-virus terutama
diperuntukkan bagi mereka yang sistem kekebalannya sudah kurang
terhadap virus.
Obat anti virus untuk HIV atau AIDS terbagi 4
Penghambat Fusi seperti Enfuvirtide
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g p
Penghambat Nukleosida pengubahtranscriptase seperti Didanosine, Lamivudine,Stavudine, Zidovudine
Penghambat HIV Protease seperti Ritonavir
Penghambat Non-Nukleosida pengubahTransciptase seperti Nevirapine
2. Infeksi virus Herpes 1. Infeksi HSV 1 : Asiklovir memberikan hasil yang
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baik untuk infeksi oral-labial. Pada HSV ensefalitis,pemberi an asiklovir iv dapat meningkatkan survivalrate.Untuk HSV 1 yang menimbulkan kerato-konjungtivitis, dapat diberikan anti virus lokal pada
mata seperti idoksuridin 0.1%.
2. Infeksi HSV 2 ; tipe ini biasanya menimbulkan herpesgenitalis. Bentuk primer dari herpse genitalis dapatdiobati dengan asiklovir yang menghasilkan
penyembuhan dan hilangnya rasa nyeri lebih cepat.Bentuk herpes genitalis rekuren tidak dapatdihambat oleh obat asilkovir. Pemberian oralmemberikan efek sedang. Topikal tidak efektif
3. Infeksi virus Varicella-zoster (VZV) Gejala pada anak-anak biasanya ringan dan
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tidak membutuhkan obat anti virus. Ada kalanyapenyakit memberat, tertutama pada pasien yang
disertai defisiensi imunologis. Untuk ini diberikan
asiklovir atau vidarabin secara I v selama 5-7
hari.
4. Infeksi Cytomegalovirus (CMV)
Retinitis karena CMV pada pasien AIDS diberigansiklovir, tetapi obat ini menimbulkan banyak
efek samping .