Vickerman K
Department of Zoology, University of Glasgow.
Parasitology. 1989;99 Suppl:S37-47. doi: 10.1017/s0031182000083402.
Survival of the trypanosome (Trypanosoma brucei) population in the mammalian body depends upon paced stimulation of the host's humoral immune response by different antigenic variants and serial sacrifice of the dominant variant (homotype) so that minority variants (heterotypes) can continue the infection and each become a homotype in its turn. New variants are generated by a spontaneous switch in gene expression so that the trypanosome puts on a surface coat of a glycoprotein differing in antigenic specificity from its predecessor. Homotypes appear in a characteristic order for a given trypanosome clone but what determines this order and the pacing of homotype generation so that the trypanosome does not quickly exhaust its repertoire of variable antigens, is not clear. The tendency of some genes to be expressed more frequently than others may reflect the location within the genome and mode of expression of the genes concerned and may influence homotype succession. Differences in the doubling time of different variants or in the rate at which trypanosomes belonging to a particular variant differentiate into non-dividing (vector infective) stumpy forms have also been invoked to explain how a heterotype's growth characteristics may determine when it becomes a homotype. Recent estimations of the frequency of variable antigen switching in trypanosome populations after transmission through the tsetse fly vector, however, suggest a much higher figure (0.97-2.2 x 10(-3) switches per cell per generation) than that obtained for syringe-passed infections (10(-5)-10(-7) switches per cell per generation) and it seems probable that most of the variable antigen genes are expressed as minority variable antigen types very early in the infection. Instability of expression is a feature of trypanosome clones derived from infective tsetse salivary gland (metacyclic) trypanosomes and it is suggested that high switching rates in tsetse-transmitted infections may delay the growth of certain variants to homotype status until later in the infection.
布氏锥虫种群在哺乳动物体内的存活取决于不同抗原变异体对宿主体液免疫反应的阶段性刺激，以及优势变异体（同型）的连续损耗，以便少数变异体（异型）能够继续感染，并依次成为同型。新变异体通过基因表达的自发转换产生，使得锥虫表面覆盖一层糖蛋白外壳，其抗原特异性与其前身不同。对于给定的锥虫克隆，同型以特征性顺序出现，但尚不清楚是什么决定了这种顺序以及同型产生的节奏，从而使锥虫不会迅速耗尽其可变抗原库。某些基因比其他基因更频繁表达的倾向可能反映了相关基因在基因组中的位置和表达模式，并可能影响同型的更替。不同变异体倍增时间的差异，或属于特定变异体的锥虫分化为不分裂（可感染媒介）粗短型的速率差异，也被用来解释异型的生长特征如何决定其何时成为同型。然而，最近对经采采蝇媒介传播后锥虫种群中可变抗原转换频率的估计表明，这一数字（每代每个细胞0.97 - 2.2×10⁻³次转换）比通过注射器传播感染所获得的数字（每代每个细胞10⁻⁵ - 10⁻⁷次转换）高得多，而且很可能大多数可变抗原基因在感染早期就以少数可变抗原类型表达。表达的不稳定性是源自感染性采采蝇唾液腺（循环后期）锥虫的锥虫克隆的一个特征，有人认为采采蝇传播感染中的高转换率可能会延迟某些变异体生长为同型状态，直到感染后期。
