IN The Name of GOD

BRIEFf R EVIEWS

Analysis of virokine & viroceptors and related meaning

By:Sherko naseri
MS OF MEDICAL VIROLOGY,TEHRAN UNIVERSITY OF MEDICAL SCIENSE

INTRODUCTION
Immune Evasion Immune Defense Controversy .VIROLOGY OR IMMUNOLOGY?

A point
Interestingly, a natural co-receptor mutation exists which directly influences the interaction with HIV and which is of pathogenetic relevance. A 32 bp deletion in CCR5, which abolishes the virus site of interaction, may confer partial resistance to infection with macrophage-tropic HIV-1 to individuals who carry the mutation (Huang et al., 1996b; Liu et al., 1996; Samson et al., 1996). Haplotype analyses indicate that the mutated allele originated quite recently, approximately 700 years ago in northeastern Europe. The timing and distribution of the mutation suggest that a former epidemic, which exerted enormous selective pressure against CCR5, might have facilitated the rapid distribution of the 32 bp deletion (Libert et al., 1998; Stephens et al., 1998). It has been suggested that in addition to the reduced levels of CCR5, high levels of the chemokines MIP-1a, MIP-1b and RANTES may contribute to the clinical resistance or the slow progression of the disease in certain individuals.

Origine of viruses
Viruses arose from the jumping genes and replicating extrachromosomal nucleic acid that exist in cell Viruses may have arisen from intracellular cellular parasites Which progressively acquired the charactristics of virus as they become more dependent on their host cells The multiple plausible possible suggest that some virus families have no ancestors that they share with other virus families (molecular biology and pathogenesis,virology.NORKIN).

Viral Immunomodulatory Strategies

The Innate Immune System
evasin of IFN evasin of CYTOKYNE evasin of NK cell & ADCC evasin of Complement

The Adaptive Immune system

evasion of AB evasion of cell mediated immunity(direct effect on MHC 1/2)

Ab-mediated

Not Ab mediated

Virological Idea
Whats FIELDS Sey?
STRUCTURAL ASPECTS OF VIRAL ENTRY Receptor Binding There are no simple generalizationsa bout virus receptors and how they bind with viral surface We note two broad issues here. The first is that most viruses have evolved a mechanism to avoid "getting stuck" at the cell surface when emerging from an infected cell. Many viruses simply bind weakly to their receptors, and thus can dissociatein a reasonablet ime. The virulence of polyomavirus in mice is inversely related to viral affinity for its sialoglycoconjugater eceptor The molecule used for initial attachment may be a quite widely distributed molecule, such as sialic acid or other glycans(heparansulfate for HSV-1), or it may be a quite specific protein,such as the adenovirus receptor, CAR, or the HIV-I receptor,CD4The molecule that triggers fusion or penetration is sometimes called a "coreceptor" (e.9., thechemokine receptorsf or HIV-I).

What's NORKIN say?

(molecular biology and pathogenesis,virology.NORKIN(ASM))
Cytokine and chemokine play key role in activing and regulating antiviral immune defenses. Members of the Herpes virus and Pox virus families encode cytokine receptor homologs(viroceptors) that are expressed at the cell surface. eg: K2R protein>Swine Pox Virus> decoy and inhibite of binding IL8 US28 protein>HCMV> decoy and inhibite of binding IL8 ORF74 protein>HHV8>Transmit signals in response to host chemokine Norkin mention to secreted viral cytokine homologos that likely it was which immunologists say VIROKINE! eg: UL146protein>HCMV> are agonist rather than antagonist>more leuckocyte are recruited to the infected cell,where they may facilitate dissemination of the infection

(molecular biology and pathogenesis,virology.NORKIN(ASM))

MC148R proteine> MCV(molluscomcontagiosome)>antagonist, this cytokine homologe inhibits the binding of both CXC and CC chemokine to their receptors These cytokine homologos antagonist are Non-Signaling Competitors and just binding to cell ligand Ok we now have 1.cytokine receptor homologos at cell surface(viroceptors) 2.cytokine homologos(virokine)

What's NORKIN say?

IN CONTIUE
NORKIN say :
In contrast to the viroceptors that are expressed at the cell surface,the secreted cytokine binding protein constitute a second majore class of cytokine modulator note that here we havnt no keyword homolog for definition eg: T2 protein>myxoma virus>witch mimics the bindig domain of the TNFreceptors ECRF3protein> witch binds IL8,provide an example of a soluble cytokine-binding protein encoded by a herpesvirus

P101,NORKIN

Stay with me plz .

What's virulence factors dictionary say?
BCRF3 is a ORF that by saimiri herpes virus that is a lymphotropic virus and lead to LPD in several non-human paimates. Approximately 30percent amino acid identity to mamalian chemokine BUT! NORKIN not known BCRF3 as a HOMOLOGOS cytokine

Back to

EVASION OF HOST DEFENSES VIRAL RECEPTORS

GENERAL SPECIFIC

VIROCEPTORS AND VIROKINES SHOULD HAVE HOMOLOGY

WHY HOMOLOGY?
Based on this theory that this constitution(virus gene) arose from cell genes that captured and modified in long time Questions? What's homology? If interaction can show homology? Whats your notion about 3th part of viral origin theory? Note that virulence factor dictionary say that can use these terms instead of themselves

PROVED HOMOLOGIES
VIL10:H(84%)M(70%) VIL6:H(62%)M(?) VIL17:H(72%)M(63%) K6:39%>> HOST? K4:41%>>HOST?

GENERAL VIROLOGY(FIELDS) VIROLOGY,molecular biology and pathogenesis VIRULENCE FACTOR DICTIONARY