紋白蝶(Pieris rapae)感染顆粒體病毒後第一至第二天，病徵不顯著，但表現行 動緩
慢，身體柔軟，食慾不振，糞便柔軟，甚至於有腹瀉現象。三至四天後，體色漸 淡，
尤其是腹面微露白色，而且完全停止取食。感染四天以後，體色變成淡黃色，具 有褐
紅斑點。感染五至六天，體色變為混濁乳黃，或褐紅帶乳白色。體節膨脹，發亮 而脆
弱，但分節明顯。瀕死或已死的病蟲，經常將其前肢或後肢掛於培養皿或植物頂 部，
軀倒掛於空中，成倒V 字型或倒J 字型。罹病蟲死後不久，皮膚變褐或黑而脆弱 ；稍
碰即碎，流出白色汁液，汁夜輸燥後，體色由褐變黑。罹病蟲，一般感染後七至 八天
死亡。
罹病輕微的幼蟲，常可發育達前蛹期，但不久即死亡，體色變黑，無化蛹現象 。或有
可化蛹者，蛹體褐黑，腐爛後乾縮。若有蛹後羽化者，其發育不良，個體甚小， 全身
變黑，翅小而畸形，翅展不開，羽化不久即告死亡。
紋白蝶顆粒體病毒可侵染真皮，脂肪體及氣管被膜細胞，故屬於嗜多器官病。病 毒首
先侵入細胞核，然後擴散到細胞質，所以被視為細胞核型的病毒。
光學顯微鏡觀察組織病理變化︰感染初期，核稍為膨大，接著核繼續膨脹，細胞 亦隨
之增大。感染中期，細胞緊縮為固縮核，進而核膜破裂。末期，網組織擴散到 整個細
胞質，細胞核質與細胞質混淆不清，而且空胞完全消失，充滿著莢膜體。終致細 胞完
全破裂，釋放出莢膜體，充滿體腔。真皮和氣管被膜細胞的病理變化情形和脂肪 體細
胞的情形相仿。
紋白蝶的顆粒體病毒的莢膜體為卵形或不正卵形，長約為300nm， 寬約為200nm 。病
毒粒子為桿狀，大小約為280×350 nm。
電子顯微鏡觀察，顯示病毒粒子由病毒子座釋放出來，然後，擴散到細胞質。病 毒在
感染細胞的核內複製和發育，起初為球形，接著變為桿狀，最後，病毒粒子為蛋 白質
所包繞而成莢膜體。病毒粒子和莢膜體的蛋白質外殼，係由內質網內網狀組織所 產生
的，故網狀組織可認為病毒子座。在感染細胞中，發現有異常的莢膜體存在。
紋白蝶顆粒體病毒在感染細胞內成熟過程如下ぇ病毒粒子進行複製與病毒子座相 結合
；え赤裸病毒粒子作有規則排列；ぉ由內質網構成病毒粒子的外膜；お在病毒粒 子與
外膜間，形成內膜か蛋白質由病毒一端開始包圍，漸漸增加，致使整個病毒包繞 及が
形成莢膜體。
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The granulosi virus infecting the cabbageworm, Pieris rapace, in Taiwan
was sudied by both optical and electron microscopy. Infected larvae were
found to become progressively pale. At medial stage, the larvae changed
their color from greenish to milky yellow on the dorsal and lateral sides
while the ventral side was white. In some cases, integument of infected
larvae became mottled and shiny, and their body often slightly swelled and
softened. At last stage, the diseased larvae lost appetite and were
languid. The carcass would hang down on the top of plants or rearing
containers. Soon after death, the body darkened and turned black
entirely. The infected larvae usually survived to the prepupal or pupal
stage and died as abnormal prepupae or pupae. The internal contents of
dead prepupae were brownish and fluid. The infection could sometimes
persist till the adult stage causing the emergence of malformed moths.
The granulosis virus disease of P. rapae is a polyorganotropic disease, i.
e., the virus may infect fat body, epidermis, and tracheal matrix.
Optical microscopic observations on histopathological changes in P. rapae
revealed the following:the nuclear materials of fat body cells,
especially the nucleolus, seemed to break up and to condense into
irregular masses 24-48 hr after inoculation. Pycnotic nuclei with
condensed chromatins could be seen in the center. Sometimes, the heavily
stained nuclear materials formed a continuous or partially continuous
network near the nuclear membrane. The nuclei continued to hypertrophy
and their membranes became barely visible 72 hr after inoculation,
therefore, the whole cell increased in size. The nucleus and cytoplasm
fused 96 hr after inoculation, either as a result of the nucleus occupying
the entire cell of more probaly because the nuclear membrane was
disintegrated, and the nuclear and cytoplasmic elements were intermingled.
At 144 hr after inoculation, the hemocoel was filled with capsules as a
result of ruptures of the infected fat body cells and other susceptible
tissues. Epidermis and tracheal matrix changed histopathologically in the
same manner as fat body cells. However, the progress of infection tended
to be better synchronized in the opidermal cells and tracheal cells than
that in fat body cells.
The capsules of this virus are ovoid or subovoid measuring 300 nm by 200
nm. The virus particle is rod-shaped, ca. 280 × 50 nm in size.
Electron microscopic observations revealed that the virus particles arose
from the virogenic stroma near endoplasmic reticulum and were liberated
into the cytoplasm. The virus particles developed within the nuclei of
infected cells, first as spheres and then as rods. Finally, each rod
became occluded by protein occlusion to form a capsule. The virus rods,
capsules, partial of encapsulation, intimate membrane of virus,
developmental membrane of virus, multimembranous structure and ring-shaped
structure embeded in the fat body cells. Virogenic stoma showed
72 and 96 hr after inoculation, but they disappeared 20 hr after
inoculation with granulosis virus of P. rapae.
The maturation of the granulosis virus of P. rapae in the fat body cells
is proposed as follows based on electron micrographs. (1) appearance of
virus particles in association with the endoplasmic reticulum; (2) regular
stacking array of virus particles; (3) formation of outer membrane; (4)
formation of intimate membrane; (5) encapsulation; and (6) complete
capsules.