Herpes Simplex Virus Causing Necrotizing Granulomatous Lymphadenitis

Parmar, Vrajesh; Bayya, Maha; Kak, Vivek

doi:10.7759/cureus.23709

Cited by 3 publications

(2 citation statements)

References 10 publications

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“…These clues support the synapse, a key site where the functional connection between neurons occurs ( Faria-Pereira and Morais, 2022 ), whose information transmission was in chaos post infection. Alterations in synaptic signaling, in the release of neurotransmitters from presynaptic neurons, changes in binding to postsynaptic receptors, and synaptic degeneration are evident in the course of many neurodegenerative diseases ( Parmar et al., 2022 ; Peng et al., 2022 ; Wang et al., 2022a ). Indeed, we found that several differentially expressed proteins were involved in the pathways of KEGG associated with neurodegenerative diseases, autophagy, and other signaling.…”

Section: Discussionmentioning

confidence: 99%

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

Cheng

Wang

et al. 2022

Front. Cell. Infect. Microbiol.

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Herpes simplex virus type 2 (HSV-2) is a common human pathogen that establishes lifelong latency in neurons of the nervous system. The number of severe central nervous system infections caused by the virus has increased recently. However, the pathogenesis of HSV-2 infection in the nervous system is not fully understood. Here, we demonstrated global proteomic changes in the brain tissue in BALB/c mice vaginally infected with HSV-2. Data are available via ProteomeXchange with identifier PXD034186. A total of 249 differentially expressed proteins were identified in infected brain tissue. The GO and KEGG enrichment analysis of these proteins indicated that they were mainly involved in the regulation of synapse formation and synaptic excitability. In addition, genes affecting autophagy, the development of other neurodegenerative diseases, and signaling pathways relevant to other neurologic diseases were identified. Additional experiments, comparing the brain tissue of asymptomatic and symptomatic mice showed a differential expression of proteins involved in synapse formation and synaptic transmission. Others were involved in autophagy, addiction, and signaling pathways of other neurologic diseases. These results suggest that changes in synaptic structure and function, as well as autophagy, may be related to the development of neurologic abnormalities that follow HSV-2 infection. We also identified a protein GluN2A encoded by Grin2a was continuously expressed at high levels after infection. We propose that GluN2A may be a key molecule in the pathogenesis of HSV-2-induced neurologic diseases.

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Section: Discussionmentioning

confidence: 99%

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

Cheng

Wang

et al. 2022

Front. Cell. Infect. Microbiol.

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“…Treatment of Richter Transformation depends on the histological features but usually consists of aggressive chemotherapeutic regimens with the possibility of Hematopoietic Cell Transplantation (HCT) [8] , [9] . Lymphadenitis secondary to Herpes Simplex Viral (HSV) infection is an exceedingly rare condition, with less than 20 cases in CLL/SLL patients reported in the literature to date [10] , [11] , [12] , [13] , [14] , [15] . The clinical presentation of HSV lymphadenitis is characterized by sudden widespread or local lymphadenopathy combined with fevers and sweating, often causing suspicion for Richter Transformation.…”

Section: Introductionmentioning

confidence: 99%

Necrotic herpes simplex lymphadenitis imitating Richter’s transformation in a patient with chronic lymphocytic leukemia – A case report

Smith

Thakker

Levine

et al. 2023

IDCases

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Case report: HSV lymphadenitis in immunocompromised patient with CLL

Al-Assil,

Handelsman,

Ansari

et al. 2024

Front. Oncol.

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BackgroundRichter’s transformation (RT) in chronic lymphocytic leukemia (CLL) is associated with poor prognosis and requires prompt modifications in patient care. CLL patients are susceptible to severe infections due to immune dysregulation induced by their malignancy and immunosuppressive therapies.Case presentationWe present a case of a 63-year-old man with CLL who previously achieved remission and presented with a right inguinal mass. He was diagnosed with Rai Stage I CLL with del6q, without TP53 mutation, and treated with 6 cycles of fludarabine, cyclophosphamide, and rituximab (FCR) 6 years prior. Transformed CLL was suspected based on his lymphadenopathy, elevated lactate dehydrogenase, and constitutional symptoms, but excisional biopsy unexpectedly revealed herpes simplex virus (HSV)-1 and HSV-2, indicating a diagnosis of HSV lymphadenitis concurrent with CLL relapse with no transformation but acquisition of 17p deletion consistent with clonal evolution. The patient received three courses of dexamethasone and acyclovir, leading to successful clearance of the infection, evidenced by the resolution of his B symptoms. Subsequently, he was treated for the CLL recurrence with rituximab and venetoclax, demonstrating a favorable response with significant improvement in adenopathy and resolution of lymphocytosis.DiscussionThis case highlights the possibility of reactivated dormant viral infections in the context of CLL relapse, underscoring the importance of comprehensive evaluation in CLL patients presenting with lymphadenopathy. Due to immunosuppressive defects and iatrogenic hypogammaglobulinemia, patients with CLL face an increased risk of viral infections, with HSV reactivation occurring more frequently and severely in the setting of hematologic malignancies and dysregulated T-cell immunity. Timely administration of antiviral therapy is crucial for HSV lymphadenitis to prevent rapid progression and debilitating symptoms. This case demonstrates the importance of considering atypical viral infection presentations in CLL patients and emphasizes the necessity of timely and adequate biopsies to differentiate between CLL transformation, HSV lymphadenopathy, and other causes of lymphadenopathy while avoiding unnecessarily aggressive lymphoma therapy.

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Herpes Simplex Virus Causing Necrotizing Granulomatous Lymphadenitis

Cited by 3 publications

References 10 publications

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

Necrotic herpes simplex lymphadenitis imitating Richter’s transformation in a patient with chronic lymphocytic leukemia – A case report

Case report: HSV lymphadenitis in immunocompromised patient with CLL

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