Ghiasi Homayon相关文献与解析，生知库 | 链接生命科学的每一步

In the Absence of Type-1 IFN, HSV-1 LAT Increases γ34.5 Expression and Enhances Mortality in Infected Mice

在缺乏I型干扰素的情况下，HSV-1 LAT 会增加γ34.5的表达并提高感染小鼠的死亡率。

期刊:Viruses-Basel

影响因子:3.5

doi:10.3390/v17081061

Oh, Jay J; Jaggi, Ujjaldeep; Arya, Deepak; Wang, Shaohui; Ghiasi, Homayon

The anti-apoptotic function of HSV-1 LAT in neuronal cell cultures but not its function during reactivation correlates with expression of two small non-coding RNAs, sncRNA1&2

HSV-1 LAT 在神经元细胞培养物中的抗凋亡功能（而非其在病毒再激活过程中的功能）与两种小非编码 RNA（sncRNA1 和 sncRNA2）的表达相关。

期刊:PLoS Pathogens

影响因子:4.9

doi:10.1371/journal.ppat.1012307

Oh, Jay J; Jaggi, Ujjaldeep; Tormanen, Kati; Wang, Shaohui; Hirose, Satoshi; Ghiasi, Homayon

The importance of IFNα2A (Roferon-A) in HSV-1 latency and T cell exhaustion in ocularly infected mice

IFNα2A（罗弗隆-A）在HSV-1潜伏感染小鼠和T细胞耗竭中的重要性

期刊:PLoS Pathogens

影响因子:4.9

doi:10.1371/journal.ppat.1012612

Wang, Shaohui; Jaggi, Ujjaldeep; Katsumata, Makoto; Ghiasi, Homayon

Absence of CD80 reduces HSV-1 replication in the eye and delays reactivation but not latency levels

CD80 的缺失会降低眼部 HSV-1 的复制并延缓病毒的再激活，但不会降低潜伏期水平。

期刊:Journal of Virology

影响因子:3.8

doi:10.1128/jvi.02010-23

Jaggi, Ujjaldeep; Matundan, Harry H; Oh, Jay J; Ghiasi, Homayon

Ample evidence for the presence of HSV-1 LAT in non-neuronal ganglionic cells of mice and humans

大量证据表明，HSV-1 LAT存在于小鼠和人类的非神经元神经节细胞中。

期刊:Journal of Virology

影响因子:3.8

doi:10.1128/jvi.00441-24

Wang, Shaohui; Song, Xueying; Rajewski, Alex; Santiskulvong, Chintda; Ghiasi, Homayon

Presence of CD80 and Absence of LAT in Modulating Cellular Infiltration and HSV-1 Latency

CD80 的存在和 LAT 的缺失在调节细胞浸润和 HSV-1 潜伏中的作用

期刊:Viruses-Basel

影响因子:3.5

doi:10.3390/v16091379

Jaggi, Ujjaldeep; Ghiasi, Homayon

A Journey through the Minefield of the Discovery and Characterization of Latency-Related RNA/Latency-Associated Transcript

探索潜伏期相关RNA/潜伏期相关转录本的发现与表征之路：一段充满荆棘的旅程

期刊:Viruses-Basel

影响因子:3.5

doi:10.3390/v16101562

Ghiasi, Homayon

发表日期：2024

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Macrophages From Latently Infected Mice Have Trained Immunity to HSV-1.

潜伏感染小鼠的巨噬细胞对 HSV-1 具有训练免疫力。

Divergent roles of macrophage subsets, FoxP3, and IL-17A in HSV-1-induced CNS pathology

巨噬细胞亚群、FoxP3 和 IL-17A 在 HSV-1 诱导的中枢神经系统病理学中发挥着不同的作用

IFNβ absence compensates for LAT functions in latency reactivation and T cell exhaustion

IFNβ 的缺失可以补偿 LAT 在潜伏感染再激活和 T 细胞耗竭中的功能。

In the Absence of Type-1 IFN, HSV-1 LAT Increases γ34.5 Expression and Enhances Mortality in Infected Mice

在缺乏I型干扰素的情况下，HSV-1 LAT 会增加γ34.5的表达并提高感染小鼠的死亡率。

The anti-apoptotic function of HSV-1 LAT in neuronal cell cultures but not its function during reactivation correlates with expression of two small non-coding RNAs, sncRNA1&2

HSV-1 LAT 在神经元细胞培养物中的抗凋亡功能（而非其在病毒再激活过程中的功能）与两种小非编码 RNA（sncRNA1 和 sncRNA2）的表达相关。

The importance of IFNα2A (Roferon-A) in HSV-1 latency and T cell exhaustion in ocularly infected mice

IFNα2A（罗弗隆-A）在HSV-1潜伏感染小鼠和T细胞耗竭中的重要性

Absence of CD80 reduces HSV-1 replication in the eye and delays reactivation but not latency levels

CD80 的缺失会降低眼部 HSV-1 的复制并延缓病毒的再激活，但不会降低潜伏期水平。

Ample evidence for the presence of HSV-1 LAT in non-neuronal ganglionic cells of mice and humans

大量证据表明，HSV-1 LAT存在于小鼠和人类的非神经元神经节细胞中。

Presence of CD80 and Absence of LAT in Modulating Cellular Infiltration and HSV-1 Latency

CD80 的存在和 LAT 的缺失在调节细胞浸润和 HSV-1 潜伏中的作用

A Journey through the Minefield of the Discovery and Characterization of Latency-Related RNA/Latency-Associated Transcript

探索潜伏期相关RNA/潜伏期相关转录本的发现与表征之路：一段充满荆棘的旅程