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      저자 : Kadwey, Mangala Nimbaji (검색결과 2 건)
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        Ultrastructural Changes in Midgut of CPV infected Tropical Tasar Silkworm, Antheraea mylitta (D) (Lepidoptera : Saturniidae)

        Barsagade, Deepak Deewaji,Kadwey, Mangala Nimbaji Korean Society of Sericultural Science 2010 International Journal of Industrial Entomology Vol.21 No.1

        The tropical tasar silkworms, Antheraea mylitta (D) produce famous silk 'Kosa' in central part of India. Due to outdoor rearing it became susceptible to viral infection including cytoplasmic polyhedrosis virus (CPV). The common mode of entry of cytoplasmic polyhedrosis virus is per os and cause gresserie disease to the larvae. Histopathological studies elucidated the insect CPV virus produces infective polyhedral inclusion bodies (PIBs) in the midgut cell cytoplasm of virus infected fifth instar larvae. The PIBs multiply enormously in the cytoplasm without invading the nucleus. Ultrastructural studies confirmed the pathological effects of CPV on in midgut cell cytoplasm. The multiplication of polyhedral inclusion bodies took place into the vacuoles and form virogenic stromata in the cytoplasm of cells. However, the encapsulations of polyhedral inclusion bodies into the polyhedrin protein occurred and polyhedra were released into the lumen. At the late stage of infection, cells showed the regressed cytoplasmic organelles with large vacuoles and elongated mitochondria. Hence, the horizontal transmission of CPV causing the midgut cells disintegration in the tasar silkworm, Antheraea mylitta (D) confirmed during infection.

      • KCI등재

        Ultrastructural Changes in Midgut of CPV infected Tropical Tasar Silkworm, Antheraea mylitta (D) (Lepidoptera: Saturniidae)

        ( Deepak Deewaji Barsagade ),( Mangala Nimbaji Kadwey ) 한국잠사학회 2010 International Journal of Industrial Entomology Vol.21 No.1

        The tropical tasar silkworms, Antheraea mylitta (D) produce famous silk ``Kosa`` in central part of India. Due to outdoor rearing it became susceptible to viral infection including cytoplasmic polyhedrosis virus (CPV). The common mode of entry of cytoplasmic polyhedrosis virus is per os and cause gresserie disease to the larvae. Histopathological studies elucidated the insect CPV virus produces infective polyhedral inclusion bodies (PIBs) in the midgut cell cytoplasm of virus infected fifth instar larvae. The PIBs multiply enormously in the cytoplasm without invading the nucleus. Ultrastructural studies confirmed the pathological effects of CPV on in midgut cell cytoplasm. The multiplication of polyhedral inclusion bodies took place into the vacuoles and form virogenic stromata in the cytoplasm of cells. However, the encapsulations of polyhedral inclusion bodies into the polyhedrin protein occurred and polyhedra were released into the lumen. At the late stage of infection, cells showed the regressed cytoplasmic organelles with large vacuoles and elongated mitochondria. Hence, the horizontal transmission of CPV causing the midgut cells disintegration in the tasar silkworm, Antheraea mylitta (D) confirmed during infection.

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