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Book ChapterDOI

Pathogenesis of Rift Valley fever virus in mosquitoes--tracheal conduits & the basal lamina as an extra-cellular barrier.

TL;DR: Evidence indicates the existence of a salivary gland infection barrier in Anopheles stephensi and the basal lamina may prevent access to mosquito cell surface virus receptors and help explain why anopheline mosquitoes are relatively incompetent arbovirus transmitters when compared to culicines.
Abstract: Knowledge of the fate of an arbovirus in a mosquito is fundamental to understanding the mosquito’s competence to transmit the virus When a competent mosquito ingests viremic vertebrate blood, virus infects midgut epithelial cells and replicates, then disseminates to other tissues, including salivary glands and/or ovaries The virus is then transmitted to the next vertebrate host horizontally via bite and/or vertically to the mosquito’s offspring Not all mosquitoes that ingest virus become infected or, if infected, transmit virus Several “barriers” to arbovirus passage, and ultimately transmission, have been identified in incompetent or partially competent mosquitoes, including, among others, gut escape barriers and salivary gland infection barriers The extra-cellular basal lamina around the midgut epithelium and the basal lamina that surrounds the salivary glands may act as such barriers Midgut basal lamina pore sizes are significantly smaller than arboviruses and ultrastructural evidence suggests that midgut tracheae and tracheoles may provide a means for viruses to circumvent this barrier Further, immunocytochemical evidence indicates the existence of a salivary gland infection barrier in Anopheles stephensi The basal lamina may prevent access to mosquito cell surface virus receptors and help explain why anopheline mosquitoes are relatively incompetent arbovirus transmitters when compared to culicines
Citations
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Journal ArticleDOI
08 Jul 2015-Viruses
TL;DR: The nature of the tissue barriers that arboviruses are confronted with in a mosquito vector and how they might surmount these barriers are explained.
Abstract: Arthropod-borne viruses (arboviruses) circulate in nature between arthropod vectors and vertebrate hosts. Arboviruses often cause devastating diseases in vertebrate hosts, but they typically do not cause significant pathology in their arthropod vectors. Following oral acquisition of a viremic bloodmeal from a vertebrate host, the arbovirus disease cycle requires replication in the cellular environment of the arthropod vector. Once the vector has become systemically and persistently infected, the vector is able to transmit the virus to an uninfected vertebrate host. In order to systemically infect the vector, the virus must cope with innate immune responses and overcome several tissue barriers associated with the midgut and the salivary glands. In this review we describe, in detail, the typical arbovirus infection route in competent mosquito vectors. Based on what is known from the literature, we explain the nature of the tissue barriers that arboviruses are confronted with in a mosquito vector and how arboviruses might surmount these barriers. We also point out controversial findings to highlight particular areas that are not well understood and require further research efforts.

332 citations


Cites background from "Pathogenesis of Rift Valley fever v..."

  • ...In mosquitoes that were infected with RVFV via intrathoracic injection, the sequence of infection was reversed: Viral antigen was first detected in the cells of the intussuscepted foregut and later in the cardial epithelial cells [104]....

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  • ...Abbreviations CHIKV chikungunya virus (Alphavirus, Togavirirdae) DENV1–4 dengue virus serotypes 1–4 (Flavivirus, Flaviviridae) EEEV eastern equine encephalitis virus (Alphavirus, Togavirirdae) JEV Japanese encephalitis virus (Flavivirus, Flaviviridae) LACV La Crosse virus (Orthobunyavirus, Bunyaviridae) ONNV O’nyong-nyong virus (Alphavirus, Togavirirdae) RVFV Rift Valley fever virus (Phlebovirus, Bunyaviridae) SFV Semliki Forest virus (Alphavirus, Togavirirdae) SINV Sindbis virus (Alphavirus, Togavirirdae) SLEV St. Louis encephalitis virus (Flavivirus, Flaviviridae) VEEV Venezuelan equine encephalitis virus (Alphavirus, Togavirirdae) WEEV western equine encephalitis virus (Alphavirus, Togavirirdae) WNV West Nile virus (Flavivirus, Flaviviridae) Conflicts of Interest The authors declare no conflict of interest....

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  • ...Further, orally acquired RVFV virions were observed in the basal labyrinth associated with the outer cardial epithelial cells and in the matrix associated with the inner cardial epithelial cells before being detected in cells of the intussuscepted foregut....

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  • ...In addition to dose-dependent MEB, dose-independent MEB have also been described for specific virus-vector combinations such as Rift Valley fever virus (RVFV) in Cx. pipiens and VEEV in Culex taeniopus [88,89]....

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  • ..., midgut epithelial cells, likely occurs via the tracheal system surrounding the midgut tissue [19,97]....

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Journal ArticleDOI
TL;DR: The corneal epithelial basement membrane is a highly specialized extracellular matrix that functions not only to anchor epithelial cells to the stroma and provide scaffolding during embryonic development but also during migration, differentiation, and maintenance of the differentiated epithelial phenotype.
Abstract: The corneal epithelial basement membrane (BM) is positioned between basal epithelial cells and the stroma. This highly specialized extracellular matrix functions not only to anchor epithelial cells to the stroma and provide scaffolding during embryonic development but also during migration, differentiation, and maintenance of the differentiated epithelial phenotype. Basement membranes are composed of a diverse assemblage of extracellular molecules, some of which are likely specific to the tissue where they function; but in general they are composed of four primary components--collagens, laminins, heparan sulfate proteoglycans, and nidogens--in addition to other components such as thrombospondin-1, matrilin-2, and matrilin-4 and even fibronectin in some BM. Many studies have focused on characterizing BM due to their potential roles in normal tissue function and disease, and these structures have been well characterized in many tissues. Comparatively few studies, however, have focused on the function of the epithelial BM in corneal physiology. Since the normal corneal stroma is avascular and has relatively low keratocyte density, it is expected that the corneal BM would be different from the BM in other tissues. One function that appears critical in homeostasis and wound healing is the barrier function to penetration of cytokines from the epithelium to stroma (such as transforming growth factor β-1), and possibly from stroma to epithelium (such as keratinocyte growth factor). The corneal epithelial BM is also involved in many inherited and acquired corneal diseases. This review examines this structure in detail and discusses the importance of corneal epithelial BM in homeostasis, wound healing, and disease.

199 citations

Journal ArticleDOI
08 Aug 2018-Insects
TL;DR: The conserved, innate immune pathways and specific anti-pathogenic strategies in mosquito midgut, hemolymph, salivary gland, and neural tissues for the control of pathogen propagation are discussed in detail.
Abstract: Mosquitoes live under the endless threat of infections from different kinds of pathogens such as bacteria, parasites, and viruses. The mosquito defends itself by employing both physical and physiological barriers that resist the entry of the pathogen and the subsequent establishment of the pathogen within the mosquito. However, if the pathogen does gain entry into the insect, the insect mounts a vigorous innate cellular and humoral immune response against the pathogen, thereby limiting the pathogen’s propagation to nonpathogenic levels. This happens through three major mechanisms: phagocytosis, melanization, and lysis. During these processes, various signaling pathways that engage intense mosquito–pathogen interactions are activated. A critical overview of the mosquito immune system and latest information about the interaction between mosquitoes and pathogens are provided in this review. The conserved, innate immune pathways and specific anti-pathogenic strategies in mosquito midgut, hemolymph, salivary gland, and neural tissues for the control of pathogen propagation are discussed in detail.

92 citations

Journal ArticleDOI
05 May 2010-Toxins
TL;DR: Proteases from a variety of sources (viruses, bacteria, fungi, plants, and insects) have toxicity towards insects, and these insecticidal proteases along with their evaluation and use as potential pesticides are discussed.
Abstract: Proteases from a variety of sources (viruses, bacteria, fungi, plants, and insects) have toxicity towards insects. Some of these insecticidal proteases evolved as venom components, herbivore resistance factors, or microbial pathogenicity factors, while other proteases play roles in insect development or digestion, but exert an insecticidal effect when over-expressed from genetically engineered plants or microbial pathogens. Many of these proteases are cysteine proteases, although insect-toxic metalloproteases and serine proteases have also been examined. The sites of protease toxic activity range from the insect midgut to the hemocoel (body cavity) to the cuticle. This review discusses these insecticidal proteases along with their evaluation and use as potential pesticides.

87 citations

Journal ArticleDOI
15 Mar 2011-Virology
TL;DR: New evidence is demonstrated that demonstrates how baculoviruses breach the basal lamina and establish efficient systemic infections in invertebrate and vertebrate animals.

80 citations


Cites background or methods from "Pathogenesis of Rift Valley fever v..."

  • ...Rift Valley fever, Sindbis, LaCrosse, and Dengue viruses and insect pathogens such as the baculoviruses AcMNPV and Bombyx mori nucleopolyhedrovirus (BmNPV) have been observed infecting tracheal epithelial cells followingmidgut cell infections or infecting other organs via tracheae (Bowers et al., 1995; Chandler et al., 1998; Engelhard et al., 1994; Kirkpatrick et al., 1994; Rahman and Gopinathan, 2004; Romoser et al., 2005)....

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  • ...…(BmNPV) have been observed infecting tracheal epithelial cells followingmidgut cell infections or infecting other organs via tracheae (Bowers et al., 1995; Chandler et al., 1998; Engelhard et al., 1994; Kirkpatrick et al., 1994; Rahman and Gopinathan, 2004; Romoser et al., 2005)....

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  • ...It has been reported that tracheal elements reach into the midgut cell basal lamina of insects (Romoser et al., 2005)....

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  • ...Tracheoblasts reaching into the midgut basal lamina have been observed by transmission electron microscopy (Romoser et al., 2005, 2004)....

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References
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Journal ArticleDOI
TL;DR: The use of avidin-biotin interaction in immunoenzymatic techniques provides a simple and sensitive method to localize antigens in formalin-fixed tissues.
Abstract: The use of avidin-biotin interaction in immunoenzymatic techniques provides a simple and sensitive method to localize antigens in formalin-fixed tissues. Among the several staining procedures available, the ABC method, which involves an application of biotin-labeled secondary antibody followed by the addition of avidin-biotin-peroxidase complex, gives a superior result when compared to the unlabeled antibody method. The availability of biotin-binding sites in the complex is created by the incubation of a relative excess of avidin with biotin-labeled peroxidase. During formation of the complex, avidin acts as a bridge between biotin-labeled peroxidase molecules; and biotin-labeled peroxidase molecules, which contains several biotin moieties, serve as a link between the avidin molecules. Consequently, a "lattice" complex containing several peroxidase molecules is likely formed. Binding of this complex to the biotin moieties associated with secondary antibody results in a high staining intensity.

13,480 citations

Book
31 Oct 1988
TL;DR: What do you do to start reading arboviruses epidemiology and ecology?
Abstract: What do you do to start reading arboviruses epidemiology and ecology? Searching the book that you love to read first or find an interesting book that will make you want to read? Everybody has difference with their reason of reading a book. Actuary, reading habit must be from earlier. Many people may be love to read, but not a book. It's not fault. Someone will be bored to open the thick book with small words to read. In more, this is the real condition. So do happen probably with this arboviruses epidemiology and ecology.

1,001 citations

Journal ArticleDOI
TL;DR: This review focuses on vector competence or vector efficiency, and particular attention is given to recent studies that have contributed to knowledge of intrinsic factors and mechanisms that control the ability of mosquitoes to vector arboviruses.
Abstract: that exist between the virus, the invertebrate host (vector), and the vertebrate host, each of which is influenced to varying degrees by environmental conditions. These interrela­ tionships have been reviewed elsewhere (17, 60,98, 109, 111, 113, 124) and are not discussed in depth here. Rather, this review focuses on vector competence or vector efficiency. Particular attention is given to recent studies that have contributed to our knowledge of intrinsic factors and mechanisms that control the ability of mosquitoes to vector arboviruses. No attempt is made to review transovarial transmission of arboviruses by ar­ thropods even though this is obviously an important aspect of vector com­ petence in certain arthropod-arbovi rus associations (35, 125, 140,

492 citations

Journal ArticleDOI
TL;DR: It is discovered that infection of the larval insect tracheal system (and not hemocytes, as thought previously) provides the major conduit for this virus to pass through basal laminae and to spread throughout the host.
Abstract: Baculoviruses establish systemic infections within susceptible insect hosts, even though host tissues are surrounded by basal laminae, extracellular matrices that exclude particles smaller than these viruses. Using a recombinant Autographa californica M nuclear polyhedrosis virus containing a lacZ reporter gene under the control of a constitutive promoter, we followed the progression of infection in Trichoplusia ni larvae. We discovered that infection of the larval insect tracheal system (and not hemocytes, as thought previously) provides the major conduit for this virus to pass through basal laminae and to spread throughout the host. Tracheal epidermal cells, the only known cellular components of the tracheal system, share a common lymph system. Locally these cells contact one another by interdigitating cytoplasmic extensions called epidermal feet. These two features of the tracheal system are likely to facilitate the rapid systemic spread of the virus. The findings reported here have major implications for the fields of insect pathology and biological control and usher in an important consideration regarding host-range factors.

312 citations


"Pathogenesis of Rift Valley fever v..." refers background in this paper

  • ...Baculoviruses appear to utilize a tracheal route of spread within their insect hosts [1, 5 , 12]....

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  • ...Further, the earliest evidence of nuclear polyhedrosis infection beyond the midgut of larval Trichoplusia ni was in tracheoblasts and tracheal epidermal cells associated with foci of infection in the midgut epithelium [ 5 ]....

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