病毒感染与免疫 英文 Viral infection and immunity

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III. Virus Spread in the Host
A. Local Replication and Local Spread B. Dissemination from the Portal of Entry
Multiplication in Target Organs
A. Local Replication & Local Spread
CPE
Normal cells
CPE
Cytopathic effect

※ virus inclusion bodies
In the some of virus-infected cells, round or oval patches with different color and structure can be observed at the light microscope. It is : Aggregation of virus particles Traces of the virus multiplication Virus induced cell reactants



Rabies virus inclusion bodies
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Polykaryocytes
RSV infectec cells
Measels virus infected cells
2. Steady state infection

Viral nucleic acid remain in specific host cells indefinitely; progeny virus may or may not be produced.
Neutralizing antibody

Antibodies which bind to the virus, usually to the peplomer and capsomer, and block the virus from binding and entering into host cell
III. Pathogenesis of viral infections
Pathogenesis of viral infections
A. Direct damage to infected host cells B. Immunopathological injury
A. Direct damage to infected host cells 1. Cytocidal infection
A. Horizontal transmission



Respiratory tract Alimentary canal Skin and mucous membrane Genital tract Blood: Injection, transfusion, transplantation Arthropod-borne
civet cat
B. Vertical Transmission
Through placenta congenital infections, congenital deformity Through birth canal infection of newborn
Vertical Transmission
Chronic infection Latent infection
Slow infection
Natural history of acute and persistent human infections.
A. Chronic infection
Continued presence of infectious virus following the primary infection and may include chronic or recurrent disease. Virus can be continuously detected.
Through Nerves
e.g. •Rabies virus •Herpesvirus •Poliovirus
II. Forms of viral infections
Types of Viral Infection
Acute viral infection Persistent viral infection
Latency and recurrence in herpes simplex virus infections
Cold sores caused by herpes virus type 1
Recurrence of Latent virus infections
Shingles caused by varicella-zoster virus
B. Dissemination from the Portal of Entry
Dissemination through Bloodstream

Viremia
Dissemination through Nerves
Through Bloodstream
e.g. •Poliovirus •Measles virus •Mumps virus
Viral infection and immunity
Outline


Section I Viral pathogenesis I. Transmission routes II. Forms of viral infections III. Pathogenesis of viral infections Section II Antiviral immunity
Recurrence of Latent virus infections
C. Slow virus infection
characterized
by a long preclinical period extending for months or years from the time of exposure subacute progressive caused by : Lentivirus (HIV) unconventional virus ( prion).
Features : • Commonly induced by enveloped virus • Virus release by budding child virus • New antigens may be produced----so, the infected cells may be attacked by host immune system
I. Innate immunity II. Specific immunity
Section 1
Viral pathogenesis
I. Transmission routes
The


route of viral infection A. Horizontal transmission B. Vertical transmission

Nonspecific Defenses
Action of IFN- α/IFN- β
act by induce the synthesis of three cell-encoded proteins
2,5-oligoadenylate synthetase
Ribonuclease
Protein kinase R
The viruses which can result in congenital infections: rubella virus cytomegalovirus (CMV) herpes simplex virus (HSV) hepatitis B virus (HBV) human immunodeficiency virus (HIV)
Interferons
NK cell
Directly lysed virus infected cells no “lag phase” Effective Early No antigen-specific



NK cell
II. Adaptive immunity
Humoral immunity
HBV, ect.
B. Latent infection
virus is usually not detectable but patient may have periodic out-breaks of disease. characterized by the lack of demonstrable infectious virus between episodes of recurrent disease HSV-1 in trigeminal ganglion HSV-2 in lumbar and sacral ganglia

Section II Antiviral immunity
IFN
Neutralizing antibody
Innate Defenses
Antiviral immunity
I. Innate immunity
Innate immune factors against viral infection
3. Integration and transformation
Integration All or part of virus nucleic acid becomes integrated into the genome at specific or any site in host cells. Outcomes: is closely related to tumor formation.
Innate Defenses
Interferons
principal source inducer IFN-α leukocyte virus/dsRNA IFN-β fibroblast virus/dsRNA IFN-γ lymphocyte antigen / mitogen
Innate Defenses
※Cytopathic effect (CPE): CPE are morphologic changes of host cells which infected by cytocidal virus, including cell swollen and round, cell lysis, or necrosis, and the formation of inclusion body, or polykaryocytes
Induction IFN- α/IFN- β IFN genes normally are not expressed The strong inducers: Viruses and doublestranded RNAs Induction is not specific for a particular virus


Skin-mucous membrane Interferons Natural killer cell macrophages
Interferon (IFN)
a heterogeneous group of glycoproteins produced by human and other animal cells after viral infection (or after exposure to other inducers.) Functions of IFNs: anti-virus, anti-tumor, immunomodulation
2. Steady state infection
3. Integration and transformation
1. Cytocidal infection
Most productive infections are called cytocidal infection because they kill the host cells.
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