Cellular resistance to arbovirus infection.

F. A. Murphy

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

When an arbovirus enters an arthropod in an infected blood meal, several mechanisms may interact to affect its life cycle and ultimate transmissibility. Intrinsic absolute failure in the establishment of infection must be contrasted with infection that is successfully established but is variably modulated in its viral yield throughout the vector's life-span. Degrees of vertebrate host resistance make this modulation a central factor in determining whether an arthropod is an important vector in nature; moreover, human intervention that affects modulating mechanisms may become a basis for disease control. In the absence of evidence of real immune resistance to arbovirus infections in arthropods, other more primitive modulating mechanisms must be considered: interferonlike substances may be formed in arthropod cells; arthropod cells may "cure" themselves by a unique endophagocytic digestion of their virus burden; homologous interference with viral replicative processes may be mediated via wild or mutant viral RNA species acting to shut down further RNA synthesis; and homologous interference may be mediated by RNA of defective-interfering virus formed earlier in infection.

Original languageEnglish (US)
Pages (from-to)197-203
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume266
StatePublished - 1975

Fingerprint

Arbovirus Infections
Arthropods
Viruses
RNA
Disease control
Viral RNA
Life cycle
Blood
Modulation
Viral Interference
Infection
Defective Viruses
Arboviruses
Life Cycle Stages
Meals
Vertebrates
Digestion

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Cellular resistance to arbovirus infection. / Murphy, F. A.

In: Annals of the New York Academy of Sciences, Vol. 266, 1975, p. 197-203.

Research output: Contribution to journalArticle

@article{80f2a23f1cd747b7b434694c1dd541b8,
title = "Cellular resistance to arbovirus infection.",
abstract = "When an arbovirus enters an arthropod in an infected blood meal, several mechanisms may interact to affect its life cycle and ultimate transmissibility. Intrinsic absolute failure in the establishment of infection must be contrasted with infection that is successfully established but is variably modulated in its viral yield throughout the vector's life-span. Degrees of vertebrate host resistance make this modulation a central factor in determining whether an arthropod is an important vector in nature; moreover, human intervention that affects modulating mechanisms may become a basis for disease control. In the absence of evidence of real immune resistance to arbovirus infections in arthropods, other more primitive modulating mechanisms must be considered: interferonlike substances may be formed in arthropod cells; arthropod cells may {"}cure{"} themselves by a unique endophagocytic digestion of their virus burden; homologous interference with viral replicative processes may be mediated via wild or mutant viral RNA species acting to shut down further RNA synthesis; and homologous interference may be mediated by RNA of defective-interfering virus formed earlier in infection.",
author = "Murphy, {F. A.}",
year = "1975",
language = "English (US)",
volume = "266",
pages = "197--203",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Cellular resistance to arbovirus infection.

AU - Murphy, F. A.

PY - 1975

Y1 - 1975

N2 - When an arbovirus enters an arthropod in an infected blood meal, several mechanisms may interact to affect its life cycle and ultimate transmissibility. Intrinsic absolute failure in the establishment of infection must be contrasted with infection that is successfully established but is variably modulated in its viral yield throughout the vector's life-span. Degrees of vertebrate host resistance make this modulation a central factor in determining whether an arthropod is an important vector in nature; moreover, human intervention that affects modulating mechanisms may become a basis for disease control. In the absence of evidence of real immune resistance to arbovirus infections in arthropods, other more primitive modulating mechanisms must be considered: interferonlike substances may be formed in arthropod cells; arthropod cells may "cure" themselves by a unique endophagocytic digestion of their virus burden; homologous interference with viral replicative processes may be mediated via wild or mutant viral RNA species acting to shut down further RNA synthesis; and homologous interference may be mediated by RNA of defective-interfering virus formed earlier in infection.

AB - When an arbovirus enters an arthropod in an infected blood meal, several mechanisms may interact to affect its life cycle and ultimate transmissibility. Intrinsic absolute failure in the establishment of infection must be contrasted with infection that is successfully established but is variably modulated in its viral yield throughout the vector's life-span. Degrees of vertebrate host resistance make this modulation a central factor in determining whether an arthropod is an important vector in nature; moreover, human intervention that affects modulating mechanisms may become a basis for disease control. In the absence of evidence of real immune resistance to arbovirus infections in arthropods, other more primitive modulating mechanisms must be considered: interferonlike substances may be formed in arthropod cells; arthropod cells may "cure" themselves by a unique endophagocytic digestion of their virus burden; homologous interference with viral replicative processes may be mediated via wild or mutant viral RNA species acting to shut down further RNA synthesis; and homologous interference may be mediated by RNA of defective-interfering virus formed earlier in infection.

UR - http://www.scopus.com/inward/record.url?scp=0016586032&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0016586032&partnerID=8YFLogxK

M3 - Article

VL - 266

SP - 197

EP - 203

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -