Host-Dependent Differences in Replication Strategy of the Sulfolobus Spindle-Shaped Virus Strain SSV9 (a.k.a., SSVK1): Infection Profiles in Hosts of the Family Sulfolobaceae
Host-Dependent Differences in Replication Strategy of the Sulfolobus Spindle-Shaped Virus Strain SSV9 (a.k.a., SSVK1): Infection Profiles in Hosts of the Family Sulfolobaceae
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DOI：
10.3389/fmicb.2020.01218
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发表时间：
2020-07-14
影响因子：
5.2
通讯作者：
Stedman, Kenneth Mark
中科院分区：
文献类型：
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作者：
Ceballos, Ruben Michael;Drummond, Coyne Gareth;Stedman, Kenneth Mark
梭形病毒（SSV）系统已成为研究嗜热病毒生物学的一个模型，包括古细菌宿主-病毒相互作用和生物地理学。有几个因素使得SSV系统适合研究古细菌的遗传机制（如crispr）以及高温酸性环境下病毒与宿主的相互作用。以前，我们报道了ssv对异域宿主和同域宿主表现出不同的感染性。我们还注意到病毒株SSV9（又名SSVK1）的宿主范围很广。几十年来，ssv被描述为“非裂解”双链DNA病毒，它感染sulfolobusus属的物种，并通过出芽而不是宿主裂解释放病毒粒子。在这项研究中，我们证明了ssv在草坪上的“晕”实验和液体培养感染实验中感染了代表多个亚砜菌科属的宿主。生长曲线分析支持SSV9病毒粒子释放导致细胞裂解的假设。虽然SSV9似乎可以裂解异域宿主，但在一个同域宿主上，SSV9表现出典型的非裂解性病毒释放，这是历史上报道的ssv。因此，SSV9类lytic行为的本质可能是由异源进化驱动的。ssv9感染的宿主生长特征似乎不是由感染的多重性（MOI）驱动的。与其他ssv（即SSV1）相比，SSV9在高温、低pH环境中的稳定性更高，可能有助于提高传输速率。然而，SSV9感染的高传播率和相对毒力似乎都不会改变易感宿主的复制谱。虽然已知CRISPR-Cas系统在原核生物中提供对病毒感染的保护，但没有报道称crispr是病毒复制策略的决定因素。SSV9 lytic样行为的机制仍然未知，是正在进行的研究的主题。这些结果表明，可能由异源进化产生的遗传因素介导了特定ssv -宿主菌株配对的不同病毒-宿主生长谱。
TheSulfolobusSpindle-shaped Virus (SSV) system has become a model for studying thermophilic virus biology, including archaeal host-virus interactions and biogeography. Several factors make the SSV system amenable to studying archaeal genetic mechanisms (e.g., CRISPRs) as well as virus-host interactions in high temperature acidic environments. Previously, we reported that SSVs exhibited differential infectivity on allopatric vs. sympatric hosts. We also noticed a wide host range for virus strain SSV9 (a.k.a., SSVK1). For decades, SSVs have been described as "non-lytic" double-stranded DNA viruses that infect species of the genusSulfolobusand release virions via budding rather than host lysis. In this study, we show that SSVs infect hosts representing more than one genus of the familySulfolobaceaein spot-on-lawn "halo" assays and in liquid culture infection assays. Growth curve analyses support the hypothesis that SSV9 virion release causes cell lysis. While SSV9 appears to lyse allopatric hosts, on a single sympatric host, SSV9 exhibits canonical non-lytic viral release historically reported SSVs. Therefore, the nature of SSV9 lytic-like behavior may be driven by allopatric evolution. The SSV9-infected host growth profile does not appear to be driven by multiplicity of infection (MOI). Greater stability of SSV9 vs. other SSVs (i.e., SSV1) in high temperature, low pH environments may contribute to higher transmission rates. However, neither higher transmission rate nor relative virulence in SSV9 infection seems to alter replication profile in susceptible hosts. Although it is known that CRISPR-Cas systems offer protection against viral infection in prokaryotes, CRISPRS are not reported to be a determinant of virus replication strategy. The mechanisms underlying SSV9 lytic-like behavior remain unknown and are the subject of ongoing investigations. These results suggest that genetic elements, potentially resulting from allopatric evolution, mediate distinct virus-host growth profiles of specific SSV-host strain pairings.