Elsberg syndrome, or HSV-2 lumbosacral radiculitis, is a rare and underrecognized neurologic condition that mimics cauda equina syndrome (CES). It typically presents with symptoms such as urinary retention, saddle ane...Elsberg syndrome, or HSV-2 lumbosacral radiculitis, is a rare and underrecognized neurologic condition that mimics cauda equina syndrome (CES). It typically presents with symptoms such as urinary retention, saddle anesthesia, and bowel incontinence. This case report describes a 59-year-old immunosuppressed male with idiopathic pulmonary fibrosis who developed Elsberg syndrome due to re-activation of latent HSV-2. The patient experienced progressive lower extremity sensory deficits and genitourinary dysfunction, culminating in a vesiculopustular rash. Diagnosis was confirmed via cerebrospinal fluid analysis and PCR testing of skin lesions. Despite early imaging findings being unremarkable, subsequent MRI revealed enhancement of the conus medullaris and cauda equina. Treatment with intravenous acyclovir, corticosteroids, and supportive therapy led to gradual functional improvement, though sensory deficits and neuropathy persisted. This case highlights the diagnostic challenges and importance of clinical suspicion for HSV-2 reactivation in immunosuppressed patients, as well as considerations for long-term symptom management.展开更多
Herpes simplex virus 2(HSV-2)is a major pathogen causing neonatal herpes and increasing the risk of human immunodeficiency virus 1(HIV-1)infection.However,the mechanisms underlying host restriction of HSV-2 infection ...Herpes simplex virus 2(HSV-2)is a major pathogen causing neonatal herpes and increasing the risk of human immunodeficiency virus 1(HIV-1)infection.However,the mechanisms underlying host restriction of HSV-2 infection are still not fully understood.The ubiquitously expressed transcript isoform 2(UXT-V2),anα-type prefoldin protein,functions as a versatile transcription factor associated with numerous human tumors,but its role in viral infection remains unclear.In this study,we found that ectopic expression of UXT-V2 significantly inhibited HSV-2 replication,while knockout of endogenously expressed UXT-V2 promoted HSV-2 proliferation.Further analysis revealed that UXT-V2 restricts HSV-2 replication independent of its role in regulating NF-κB.In the context of HSV--2 infection or in viral glycoprotein B(gB)-transfected cells,UXT-V2 facilitates K48-linked ubiquitination of gB,leading to its degradation via the proteasome pathway,thereby inhibiting viral replication.Furthermore,we identified that UXT-V2 interacts with gB,recruiting the E3 ligase TRIM21 to facilitate K48-linked ubiquitination of gB.HSV-2,in turn,reduces the abundance of UXT-V2 proteins both in vitro and in mice,highlighting the complexity of HSV-2-host interactions.Collectively,our findings,for the first time,demonstrate an anti-HSV-2 role of UXT-V2,unveiling a novel host immune defense mechanism involved in regulating glycoprotein homeostasis.展开更多
文摘Elsberg syndrome, or HSV-2 lumbosacral radiculitis, is a rare and underrecognized neurologic condition that mimics cauda equina syndrome (CES). It typically presents with symptoms such as urinary retention, saddle anesthesia, and bowel incontinence. This case report describes a 59-year-old immunosuppressed male with idiopathic pulmonary fibrosis who developed Elsberg syndrome due to re-activation of latent HSV-2. The patient experienced progressive lower extremity sensory deficits and genitourinary dysfunction, culminating in a vesiculopustular rash. Diagnosis was confirmed via cerebrospinal fluid analysis and PCR testing of skin lesions. Despite early imaging findings being unremarkable, subsequent MRI revealed enhancement of the conus medullaris and cauda equina. Treatment with intravenous acyclovir, corticosteroids, and supportive therapy led to gradual functional improvement, though sensory deficits and neuropathy persisted. This case highlights the diagnostic challenges and importance of clinical suspicion for HSV-2 reactivation in immunosuppressed patients, as well as considerations for long-term symptom management.
基金supported by the National Natural Science Foundation of China(82472272 and 82171736)the National Key Research and Development Program of China(2022YFC2304301 and 2023YFC2306600).
文摘Herpes simplex virus 2(HSV-2)is a major pathogen causing neonatal herpes and increasing the risk of human immunodeficiency virus 1(HIV-1)infection.However,the mechanisms underlying host restriction of HSV-2 infection are still not fully understood.The ubiquitously expressed transcript isoform 2(UXT-V2),anα-type prefoldin protein,functions as a versatile transcription factor associated with numerous human tumors,but its role in viral infection remains unclear.In this study,we found that ectopic expression of UXT-V2 significantly inhibited HSV-2 replication,while knockout of endogenously expressed UXT-V2 promoted HSV-2 proliferation.Further analysis revealed that UXT-V2 restricts HSV-2 replication independent of its role in regulating NF-κB.In the context of HSV--2 infection or in viral glycoprotein B(gB)-transfected cells,UXT-V2 facilitates K48-linked ubiquitination of gB,leading to its degradation via the proteasome pathway,thereby inhibiting viral replication.Furthermore,we identified that UXT-V2 interacts with gB,recruiting the E3 ligase TRIM21 to facilitate K48-linked ubiquitination of gB.HSV-2,in turn,reduces the abundance of UXT-V2 proteins both in vitro and in mice,highlighting the complexity of HSV-2-host interactions.Collectively,our findings,for the first time,demonstrate an anti-HSV-2 role of UXT-V2,unveiling a novel host immune defense mechanism involved in regulating glycoprotein homeostasis.
