2019 年冠状病毒病 - COVID-19
中文名称
通路描述
2019 年冠状病毒病(COVID-19)是由严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的一种高度传染性的呼吸道疾病。SARS-CoV-2 通过血管紧张素转换酶 2(ACE2)受体感染肺泡上皮细胞(主要是肺泡上皮 2 型细胞)。当 SARS-CoV-2 占据 ACE2 时,由于 ACE2 介导的降解减少,导致血清中游离血管紧张素 II(Ang II)水平增加,促进通过血管紧张素 II 型 1 受体(AT1R)激活 NF-κB 途径,随后产生白细胞介素 -6(IL-6)。SARS-CoV-2 还激活先天免疫系统;巨噬细胞刺激导致促炎细胞因子(包括 IL-6)的过度产生,引发“细胞风暴”,导致全身性炎症反应综合征和多器官功能障碍。补体激活、失调的中性粒细胞增多、内皮损伤和凝血异常似乎相互交织,以驱动 COVID-19 的严重特征。
英文描述
Coronavirus disease of 2019 (COVID-19) is a highly contagious respiratory infection that is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 infects alveolar epithelial cells [mainly alveolar epithelial type 2 (AEC2) cells] through the angiotensin-converting enzyme 2 (ACE2) receptor. Upon the occupancy of ACE2 by SARS-CoV-2, the increased serum level of free Angiotensin II (Ang II) due to a reduction of ACE2-mediated degradation promotes activation of the NF-kappa B pathway via Ang II type 1 receptor (AT1R), followed by interleukin-6 (IL-6) production. SARS-CoV-2 also activates the innate immune system; macrophage stimulation triggers the overproduction of pro-inflammatory cytokines, including IL-6, and the "cytokine storm", which results in systemic inflammatory response syndrome and multiple organ failure. The combined effects of complement activation, dysregulated neutrophilia, endothelial injury, and hypercoagulability appear to be intertwined to drive the severe features of COVID-19.
所含基因
236 个基因
ACE
ACE2
ADAM17
ADAR
AGTR1
C1QA
C1QB
C1QC
C1R
C1S
C2
C3
C3AR1
C4A
C4B
C5
C5AR1
C6
C7
C8A
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C8G
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CASP1
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CFD
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CHUK
CSF2
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CXCL10
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CYBB
EGFR
EIF2AK2
F13A1
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F2
FAU
FCGR2A
FGA
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FGG
FOS
HBEGF
IFIH1
IFNA1
IFNA10
IFNA13
IFNA14
IFNA16
IFNA17
IFNA2
IFNA21
IFNA4
IFNA5
IFNA6
IFNA7
IFNA8
IFNAR1
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IFNB1
IKBKB
IKBKE
IKBKG
IL12A
IL12B
IL1B
IL2
IL6
IL6R
IL6ST
IRAK1
IRAK4
IRF3
IRF9
ISG15
JAK1
JUN
LOC102723407
LOC102723573
LOC102724737
MAP3K7
MAPK1
MAPK10
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MAPK13
MAPK14
MAPK3
MAPK8
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MAS1
MASP1
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MBL2
MMP1
MMP3
MX1
MX2
MYD88
NFKB1
NFKBIA
NFKBIB
NLRP3
NRP1
OAS1
OAS2
OAS3
P3R3URF-PIK3R3
PIK3CA
PIK3CB
PIK3CD
PIK3R1
PIK3R2
PIK3R3
PLCG1
PLCG2
PRKCA
PRKCB
PRKCG
RELA
RIGI
RPL10
RPL10A
RPL10L
RPL11
RPL12
RPL13
RPL13A
RPL14
RPL15
RPL17
RPL18
RPL18A
RPL19
RPL21
RPL22
RPL22L1
RPL23
RPL23A
RPL24
RPL26
RPL26L1
RPL27
RPL27A
RPL28
RPL29
RPL3
RPL30
RPL31
RPL32
RPL34
RPL35
RPL35A
RPL36
RPL36A
RPL36A-HNRNPH2
RPL36AL
RPL37
RPL37A
RPL38
RPL39
RPL39L
RPL3L
RPL4
RPL41
RPL5
RPL6
RPL7
RPL7A
RPL8
RPL9
RPLP0
RPLP1
RPLP2
RPS10
RPS10-NUDT3
RPS11
RPS12
RPS13
RPS14
RPS15
RPS15A
RPS16
RPS17
RPS18
RPS19
RPS2
RPS20
RPS21
RPS23
RPS24
RPS25
RPS26
RPS27
RPS27A
RPS27L
RPS28
RPS29
RPS3
RPS3A
RPS4X
RPS4Y1
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RPS5
RPS6
RPS7
RPS8
RPS9
RPSA
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RSL24D1
SELP
STAT1
STAT2
STAT3
STING1
SYK
TAB2
TBK1
TLR2
TLR3
TLR4
TLR7
TLR8
TMPRSS2
TNF
TNFRSF1A
TRAF3
TRAF6
TYK2
UBA52
VWF