我查到的資料是
As we saw for bacteria (cf. p. 255), viruses can block
complement-mediated induction of the inflammatory
response and thereby prevent viral killing. Pox viruses
encode a complement control protein VCP (IMP)
which binds C3b and C4b, making both the classical
(C 4b2a) and alternative (C3bBb) C3 convertases susceptible
to factor I-mediated destruction. For its part,
herpes simplex type 1 subverts the complement cascade
by virtue of its surface glycoprotein C which
binds C3b, interfering with its interaction with C5 and
properdin.
Several viruses utilize complement receptors to gain
entry into cells, especially since engagement of the
complement receptor alone on a macrophage is a feeble
activator of the respiratory burst. Flavivirus coated
with iC3b enters through the CR3 receptors. Members
of the regulators of the complement activation (RCA)
family are used as cellular receptors for various viruses,
such as CD46 (membrane cofactor protein) by
measles virus and human herpes virus-6 (HHV-6), and
CD55 (decay accelerating factor) used by echoviruses
and coxsackie viruses. As noted previously, EBV infects
B-cells by binding to the CR2 surface receptors.
Ominously, HIV coated with antibody and complement
is more virulent than unopsonized virus.
出處Roitt’s Essential Immunology 10th Edition
(Ivan M. Roitt, 2001;Chapter13:p268)
※ 引述《amandaL (雅嫚達)》之銘言：
: 我記得B-cell免疫缺失的是胞外細菌感染，所以這題的答案我選了(a)，
: 因為與病毒感染相關的通常是T-cell的cellular immunity，
: 而題目也和我查到的資料有點出入... 什麼叫做「阻斷」病毒入侵寄主細胞？
: Janeway我查到唯一和病毒vs.Ab有關的資料，是說明抗體會bind在virus的
: 外套膜上的蛋白，這個應該和病毒正在入侵寄主細胞時「阻斷」病毒的入侵有點出入吧？
: 不知道友沒有人也有相同的疑點... 或是可以幫忙修正我的邏輯的...
: 謝謝
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