Artikel Jurnal :: Kembali

Artikel Jurnal :: Kembali

the autoimmune mechanism in dengue hemorrhagic fever / Soroy Lardo, Marsetyawan HNE. Soesatyo; Juffrie; Sitti R. Umniyati

Nomor Panggil 610 IJIM 50:1 (2018)
Pengarang
Pengarang lain/Kontributor
Penerbitan Jakarta: Interna Publishing, 2018
 Abstrak
ABSTRAK
The immune response of dengue fever/dengue hemorrhagic fever is a series of immunopathogenesis processes starting from viral infection to the target on monocytes and macrophages. It may consequently cause a cascade of viremia in the circulation that stimulates the afferent, efferent, and effector mechanism by the interaction of the humoral and complement system. The cascade results in inflammatory substance that will affect capillary permeability and activate coagulation factors leading to further effects on endothelial level. The mechanism involving pathogenesis of DHF/DSS is still vague. So far, a theory of heterologous infection has been developed, which explains that on second infection, there is subneutralization that induce viral replication. The autoimmune mechanism development leads to the better understanding of DHF. It also explains the autoimmune response of the viral infection, which consists of molecular mimicry, bystander activation and viral persistence. The development of the autoimmune pathomechanism is related to the role of autoantibody and endothelial dysfunction that may have role in worsening DHF.
 Info Lainnya
Sumber PengataloganLibUI eng rda
ISSN01259326
Majalah/JurnalThe Indonesian Journal of Internal Medicine
VolumeVol. 50, No. 1, Januari 2018: Hlm. 70-79
Tipe Konten text
Tipe Media unmediated
Tipe Carrier volume
Akses Elektronik
Institusi Pemilik Universitas Indonesia
Lokasi Perpustakaan UI, Lantai 4, R. Koleksi Jurnal
  • Ketersediaan
  • Ulasan
  • Sampul
Nomor Panggil No. Barkod Ketersediaan
610 IJIM 50:1 (2018) 03-18-990567107 TERSEDIA
Ulasan:
Tidak ada ulasan pada koleksi ini: 20470698
ABSTRAK
The immune response of dengue fever/dengue hemorrhagic fever is a series of immunopathogenesis processes starting from viral infection to the target on monocytes and macrophages. It may consequently cause a cascade of viremia in the circulation that stimulates the afferent, efferent, and effector mechanism by the interaction of the humoral and complement system. The cascade results in inflammatory substance that will affect capillary permeability and activate coagulation factors leading to further effects on endothelial level. The mechanism involving pathogenesis of DHF/DSS is still vague. So far, a theory of heterologous infection has been developed, which explains that on second infection, there is subneutralization that induce viral replication. The autoimmune mechanism development leads to the better understanding of DHF. It also explains the autoimmune response of the viral infection, which consists of molecular mimicry, bystander activation and viral persistence. The development of the autoimmune pathomechanism is related to the role of autoantibody and endothelial dysfunction that may have role in worsening DHF.