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Purnomo Hadi Mikrobiologi FK UNDIP

Keberhasilan

infeksi virus menyebakan penyakit sangat dipengaruhi oleh efektifitas kerja sistem imun

Dua

jenis sistem imun yang bekerja melawan infeksi virus:


1. SI Innate (non-spesifik)
2. SI Adaptif (spesifik)

General:

mechanical chemical Inflamation Phagocytosis


Special:

Interferons

natural killer (NK) cells.

Merupakan

protein yg disintesis dan disekresi akibat respon sel yg diinfeksi virus produksi: dsRNA yg dibentuk, baik oleh virus jenis dsRNA, maupun virus ssRNA yg sedang berreplikasi.

Pemicu

Peran: Melindungi sel yg berdekatan Aktivasi imunitas yg dimediasi oleh sel T.

1.

Alpha- dan beta- (- dan -) interferons: diproduksi oleh kebanyakan sel yg diinfeksi virus.

2.

gamma- (-) interferon: terutama diproduksi oleh sel T dan sel NK ketika diinduksi oleh molekulmolekul tertentu (mis. interleukin-2) yg dilepaskan selama respon imun.

Activation of genes that encode antiviral proteins, such as dsRNA-dependent protein kinase R and RNase L. Stimulation of production of major histocompatibility (MHC) class I molecules and proteasome proteins; these molecules enhance the presentation of viral peptides on the infected cell surface to T cells. Activation of NK cells Induction of apoptosis

Many

viruses produce proteins that inhibit either the production of interferons or their activities. The NS1 protein of influenza A virus and the NS3-4A protein of hepatitis C virus block pathways involved in interferon production. Some viruses, such as poliovirus, prevent the synthesis of interferons as a result of a general inhibition of cell gene expression

NK cells are present throughout the body, but mainly in the blood. They recognize changes in the surface molecules of virus-infected cells as a result of infection, though they do not recognize specific antigens, unlike B cells and T cells. After recognizing virus-infected cells as target cells, NK cells are able to bind to them and kill them NK cells kill their target cells either by releasing perforins, which are proteins that are inserted into the plasma membrane of the virus-infected cell, or by inducing apoptosis. Also, on binding to infected cells, NK cells release interferon.

The

presence of HIV particles in the blood alters the expression of a number of molecules on the surface of NK cells.

This

reduces the efficiency of NK cell activities, including the ability to kill virus-infected cells and to secrete interferon.

An important outcome of virus infection in a vertebrate host is the development of a virusspecific immune response triggered by the virus antigens. Regions of antigens known as epitopes bind to specific receptors on lymphocytes, activating cascades of events that result in the immune response. Lymphocytes are the key cells in specific immune responses. There are two classes of lymphocyte:

B lymphocytes (B cells) and T lymphocytes (T cells).

Virus-specific antibody can coat both virions and virus-infected cells, and this may lead to their destruction by a variety of mechanisms. A number of cell types in the immune system have receptors for the Fc region of IgG), allowing these cells to attach to antibody-coated virions and cells. Cell types that have IgG Fc receptors include:

neutrophils and macrophages (these cell types are

phagocytes and may phagocytose the antibody-coated materials; they may also kill cells without phagocytosing them) NK cells (these cells may kill virus-infected cells by insertion of perforins into their membranes)

Another outcome of antibody binding to virus antigens is the activation of complement:

1.

Insertion of complement protein complexes into membranes of virus-infected cells and enveloped virions, leading to destruction of these cells and virions. Virions become coated with complement proteins: There are receptors for some of these proteins on neutrophils and macrophages, so phagocytosis of virions is enhanced.

2.

Antibody binding virions effect in neutralization of infectivity, by a variety of mechanisms: Release of nucleic acid from virions. Prevention of virion attachment to cell receptors. Release of virions that have attached to cell receptors. Inhibition of entry into the cell. Inhibition of genome uncoating

Helper T cells (CD4 cells): play essential roles in the initiation of immune responses, for example in triggering B cells to develop into antibodysecreting cells and in the maturation of cytotoxic T cells. Cytotoxic T cells (CD8 cells): kill virus-infected cells. There is a requirement for viral antigens to be expressed at the surface of target cells. The antigens may be virion surface proteins (e.g. envelope glycoproteins) though often the target antigens are internal virion components, or even nonstructural proteins. Cytotoxic T cells specific for early virus proteins may destroy virus-infected cells long before any infectious virus is produced.

Inhibition

of MHC-I-Restricted Antigen Presentation: adenoviruses, herpesviruses Inhibition of MHC-II-Restricted Antigen Presentation: herpesviruses, papillomaviruses Inhibition of Natural Killer Cell Lysis: poxvirus Molluscum contagiosum, HHV-5 (CMV), herpesviruses Interference with Apoptosis: tumor virus Inhibition of Cytokine Action: Epstein Barr virus, Vaccinia virus, Poliovirus, Reovirus

The

most frequent means of subverting the humoral response is by highfrequency genetic variation of the B-cell epitopes on antigens to which antibodies bind. This is only possible for viruses that are genetically variable (e.g., influenza virus and HIV). Herpesviruses use alternative strategies such as encoding viral Fc receptors to prevent Fc-dependent immune activation.