VARICELLA

Varicella = chickenpox, merupakan infeksi

primer
Rekuren zoster (shingles)
 STRUKTUR
Struktur dan morfologi identik dengan
herpesvirus, tetapi antigen berbeda
Hanya memiliki 1 serotipe
Virus yang sama menyebabkan varicella dan
zoster
Manusia merupakan hospes alami
 The core region of varicellazoster virus (VZV)
consists of a linear double-stranded DNA
genome.

The genome is surrounded by a complex

nucleocapsid composed of 162 capsomeres,
which form the 80120 nm icosahedron.

VZV also possesses an amorphous proteinaceous

tegument, which bridges the lipid envelope and
the nucleocapsid.
 REPLIKASI
Penempelan virus pada permukaan sel

Entry

Uncoated

Genome DNA masuk nukleus

Konfigurasi genom DNA berubah : linear sirkular

mRNA virus ditranskripsikan oleh RNA polimerase host translasi mjd protein
nonstruktural (di sitoplasma) : DNA polimerase dan Thymidine kinase

DNA polimerase mereplikasi genome DNA virus protein struktural transport ke

nukleus

Penyusunan virion

Virion mendapat envelope melalui Budding pd membran nukleus

Keluar sel melalui tubulus atau vakuola

 TRANSMISI & EPIDEMIOLOGI
Transmisi melalui droplet respiratori, kontak
langsung dengan lesi
Sangat menular pada anak-anak

Terdapat VZV infeksius pada vesikel zoster, dan

dapat ditransmisikan ke anak-anak (melalui
kontak) dan menyebabkan varicella
PATOGENESIS
PATOGENESIS
 A model of the pathogenesis of primary VZV infection.
T cells within the local lymphoid tissue of the respiratory tract may
become infected by transfer of VZV from its initial site of
inoculation in respiratory epithelial cells.
T cells may then transport the virus to the skin immediately and
release infectious VZV.
The remainder of the 1021-d incubation period appears to be the
interval required for VZV to overcome the innate IFN- response in
enough epidermal cells to create the typical vesicular lesions
containing cell-free virus at the skin surface.
The signaling of enhanced IFN- production in adjacent skin cells
may prevent a rapid, uncontrolled cellcell spread of VZV.
Secondary crops of varicella lesions may result when T cells traffic
through early stage cutaneous lesions become infected and
produce a secondary viremia.
Intact host immune responses appear to be required to trigger up-
regulation of adhesion molecules, facilitating the clearance of VZV
by adaptive immunity
 MANIFESTASI KLINIS
1. Varicella
Masa inkubasi 14-21 hari
Gejala prodromal : demam, malaise
Kemudian muncul bercak papulovaskular
2. Zoster
Berupa vesikel yang nyeri pada saraf sensoris pada
kepala dan badan
Nyeri dapat hilang dalam 1 mgg
Dapat terjadi poszozter neuralgia
 PEMERIKSAAN LABORATORIUM
Tzanck smear