Alzheimer's disease (AD) is the most common neurodegenerative disorder in older adults, characterized by progressive cognitive decline that ultimately leads to severe dementia. The primary pathophysiological hallmarks of AD include the accumulation of amyloid-β plaques, neurofibrillary tangles composed of hyperphosphorylated tau protein, synaptic dysfunction, and pronounced neuroinflammation. Although the exact relationship between neuroinflammation and AD pathogenesis remains incompletely understood, neuroinflammation is consistently recognized as an early and sustained feature of the disease. Accumulating evidence suggests that microbial infections, such as herpes simplex virus type 1, varicella-zoster virus, and Porphyromonas gingivalis, may play a role in the etiology and progression of AD and its associated neuroinflammatory processes. The gut microbiota may also contribute to AD pathogenesis through a complex communication network known as the microbiota-gut-brain axis. Dysbiosis, defined as an imbalance in the gut microbial community, may promote AD development and progression by enhancing neuroinflammation and producing microbial-derived toxic metabolites that can impair brain function. Neuroinflammation, in turn, contributes to the disruption of blood-brain barrier integrity, thereby facilitating the infiltration of peripheral immune cells and pathogens into the central nervous system. Importantly, chronic infections may lead to sustained immune activation, establishing a vicious cycle that further amplifies neuroinflammation, thus potentially accelerating AD progression. Emerging evidence highlights the interplay between systemic infections, immune dysregulation, and neurodegenerative processes, suggesting that pathogen-driven inflammation may represent a modifiable risk factor and a potential therapeutic target in AD. In this review, we examine the putative role of infectious pathogens in the development and progression of AD, with particular emphasis on the molecular pathways and key mediators involved in pathogen-triggered neuroinflammation.

Hearing loss in viral neuroinfections is poorly investigated. The present study aimed to clarify if hearing loss can develop in viral meningitis and encephalitis. An OAE (oto-acoustic emission) was measured in adult patients with viral meningitis and encephalitis on the day of admission and 30-60 days after discharge. Frequencies were categorized as Low (1, 1.5, 2 kHz), Mid (3, 4, 5 kHz), Mid-high (6, 7, 8 kHz), and High (9, 10 kHz). An OAE was measured in 41 patients with viral meningitis and 8 patients with encephalitis. Six patients with viral meningitis (15%) experienced a decrease of > 5 dB in one or more frequency categories. Twelve patients (29%) had a temporary decrease in OAE levels of more than 5 dB and 23 patients (54%) had no change in OAE levels between admission and follow-up. We found no significant differences in OAE levels from admission to follow-up between viral meningitis pathogens. In viral encephalitis, herpes simplex virus was associated with a decrease in OAE levels in all frequencies in 3 of 5 patients. Varicella zoster encephalitis was not associated with changes in OAE levels. Viral meningitis and herpes simplex encephalitis is associated with development of a sensorineural hearing loss.

Intracranial dermoid cysts are rare, benign congenital lesions originating from ectodermal remnants. Though typically asymptomatic, their rupture, although infrequent, can lead to significant neurological complications, such as chemical meningitis, vasospasm, and hydrocephalus. Imaging with computed tomography (CT) and magnetic resonance imaging (MRI) plays a crucial role in diagnosis, providing characteristic features related to the high lipid content of these lesions. An 86-year-old female presented with a 3-day history of headache, nausea, vomiting, and facial cellulitis after an arthropod bite. Concern that the facial cellulitis might have progressed and involved deeper structures prompted imaging studies. Non-contrast CT revealed an incidental ruptured pericallosal dermoid cyst with lipid material in the ventricular system. MRI confirmed the rupture, showing hyperintense lesions on T1-weighted sequences. Cerebrospinal fluid analysis indicated aseptic meningitis. The patient has been diagnosed with herpes zoster-related meningoencephalitis. Despite their rarity, ruptured intracranial dermoid cysts remain challenging due to their complex presentation. Early identification through advanced imaging is essential for guiding appropriate intervention. While complete resection is the goal, subtotal excision can be indicated when the cyst capsule adheres to critical neurovascular structures, given the low risk of recurrence and malignant transformation.

Multiple sclerosis (MS) is a complex, multifactorial neurodegenerative disease with an aetiology that is still partially elusive. Several risk factors are associated with MS development including genetic predisposition and various environmental stressors; however, recently, viral infections have gained significant attention as a crucial environmental trigger. Despite the well-established link between Epstein-Barr virus (EBV) and MS susceptibility, a single-pathogen model fails to clearly characterise the molecular cascades driving the disease, suggesting that the transition from infection to autoimmune response involves more than one viral agent. In this review we examine the speculation that the interactions among different neurotropic viruses could serve a collective causative role in MS, which is under-researched in the literature at present. We summarise contradictory evidence on the role of different viral agents, including the Herpesviridae family (Human Cytomegalovirus, EBV, Herpes Simplex Viruses HSV-1 and HSV-2, and Varicella Zoster Virus), Paramyxoviridae family (Measles Virus and Rubella Virus), Influenza virus, SARS-CoV-2, and Human Endogenous Retroviruses (HERVs). Through interplay within shared molecular pathways, immune modulation, and activation of latent infections, these viruses may collectively influence the inflammatory and demyelinating processes that characterise MS. This review evaluates the etiological role of viral interplay in MS through the cumulative and interactive effects of these pathogens. The available epidemiological, immunological, and experimental data converge on the concept that viral co-exposures act synergistically to shape MS susceptibility in genetically predisposed individuals. Characterising these viral interactions presents a new research direction for the identification of novel biomarkers and the development of preventative strategies through the targeted control of viral networks.

In the early years of the AIDS epidemic, the occurrence and potential for heterosexual transmission of human immunodeficiency virus type 1 (HIV 1) in the United States were uncertain. To better understand infection among women and the possible role of prostitution in the emerging epidemic, the Centers for Disease Control and Prevention established CDC AIDS Project 72, a multisite study of 1 410 women with recent histories of prostitution recruited from eight areas of the United States during 1986 and 1987. Participants were interviewed, examined, and tested for serologic markers of HIV 1, hepatitis B virus (HBV), syphilis, herpes simplex virus types 1 and 2 (HSV 1 and HSV 2), and human T cell lymphotropic virus types I and II (HTLV I/II). HIV 1 antibodies were detected in approximately 12% of women tested, but prevalence varied considerably across study sites. HSV 2 was the most commonly detected infection, followed by HSV 1, HBV, syphilis, HIV 1, and HTLV I/II. HIV 1, HBV, and HTLV I/II were strongly associated with injection drug use, whereas syphilis and HSV 2 followed different patterns related to sexual exposure. Among women without evidence of injection drug use, infrequent condom use during vaginal intercourse with clients was associated with HIV 1 infection. Project 72 showed that prostitution alone did not explain infection risk among these women. Injection drug use, sexual and injection networks, local prevalence of infection, and the social circumstances in which women lived and worked were also important. The project contributed to an evolving public health approach that emphasized epidemiologic evidence, cooperation with affected communities, and practical strategies for reducing risk rather than assumptions about stigmatized populations.

Herpes simplex virus (HSV) infection is a well-recognized complication of atopic dermatitis, most commonly presenting as eczema herpeticum. Deep herpes is a recently described clinicopathologic manifestation of HSV infection, characterized by viral involvement of cutaneous stromal cells with limited or absent epidermal infection, which can make diagnosis challenging when classic histopathologic findings are absent. We report a 17-year-old adolescent with severe atopic dermatitis who presented with fever and a rapidly progressive painful erosive eruption. Evaluation revealed methicillin-resistant Staphylococcus aureus (MRSA) bacteremia. Skin biopsy demonstrated a hyperplastic spongiotic epidermis with a superficial and mid-dermal inflammatory infiltrate. Although characteristic epidermotropic HSV cytopathic changes were absent, HSV-2 immunohistochemistry identified infected cells within the dermal inflammatory infiltrate, supporting a diagnosis of deep herpes. The patient demonstrated rapid clinical improvement following treatment with intravenous acyclovir and vancomycin, with cessation of new lesion formation, progressive re-epithelialization, and resolution of systemic symptoms. This case highlights deep herpes as an uncommon manifestation of HSV infection in an adolescent with severe atopic dermatitis complicated by concurrent MRSA bacteremia. Pediatricians should consider deep herpes in patients with severe atopic dermatitis who present with painful erosive eruptions and systemic symptoms, particularly when clinical findings and routine diagnostic testing are inconclusive.

Herpes zoster (HZ) typically presents with a unilateral vesicular eruption accompanied by neuropathic pain. Although pain is a characteristic feature, painless presentations may occur and can create a diagnostic challenge. We report the case of an 88-year-old woman with advanced chronic kidney disease (CKD) who developed a unilateral vesicular eruption involving the right thoracic dermatome without pain at any stage of the disease. She was not receiving immunosuppressive therapy and had no known diabetes mellitus, previous HZ, or neurological disorder. The diagnosis was made clinically based on the characteristic unilateral dermatomal distribution and morphology of the lesions. Renally adjusted oral valacyclovir was administered for seven days, with complete resolution of the cutaneous lesions within approximately one week. No postherpetic neuralgia (PHN) developed, and the patient remained completely pain-free during follow-up. This case highlights that the absence of pain should not exclude HZ, even in very elderly patients with advanced CKD. Careful recognition of the characteristic dermatomal morphology remains essential for timely diagnosis and treatment.

Guillain-Barré syndrome (GBS) is a leading cause of acquired acute neuromuscular paralysis and is an immune-mediated disorder of the peripheral nervous system (PNS). Accumulating evidence indi-cates that GBS is often preceded by infectious events that trigger autoimmune responses through mechanisms such as molecular mimicry and autoantibody production. Campylobacter jejuni remains the most common bacterial agent, but viral pathogens also contribute to the development of GBS. This review summarizes the current evidence regarding viruses as triggers of GBS, including herpes-viruses, hepatotropic viruses (A, B, C, and E), human immunodeficiency virus, Zika virus, influenza virus, varicella-zoster virus, and the coronavirus SARS-CoV-2. Emphasis is placed on laboratory test results related to viral GBS, including antiganglioside antibodies, serological markers of recent in-fection, molecular diagnostic methods, and cerebrospinal fluid analysis. From the standpoint of la-boratory medicine, both the clinical diagnosis and the distinction of GBS subtypes can be supported by the identification of recent viral infections and the detection of immunological biomarkers. How-ever, cross-reactivity, extended antibody persistence, and inadequate assay standardization frequently make it difficult to interpret laboratory test results. In patients with probable viral GBS, this review shows the diagnostic significance and limitations of routine laboratory testing. It also highlights the significance of close coordination between laboratory professionals and clinicians.

Viral hepatitis and associated liver injury represent a major global public health concern, capable of progressing to chronic liver disease, cirrhosis, and hepatocellular carcinoma. This review systematically summarizes classic hepatotropic viruses-including hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis A virus (HAV)-as well as atypical liver-injury pathogens such as hepatitis E virus (HEV), hepatitis D virus (HDV), human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV), and yellow fever virus, with respect to their molecular biological characteristics, global epidemiological profiles, infection and pathogenic mechanisms, and strategies for diagnosis, treatment, and prevention. Particular emphasis is placed on the genomic architecture and replication cycles of these viruses, host immune responses and viral evasion strategies, key molecular events driving disease progression, and recent advances and remaining challenges in vaccination, direct-acting antiviral therapy, and public health interventions. By integrating evidence across multiple pathogens, this review aims to provide a systematic theoretical reference for the precise prevention and control of viral hepatitis and associated liver injury, as well as for the optimization of clinical diagnosis and management.

Australia used the live attenuated herpes zoster vaccine (ZVL, Zostavax®) for 70-79 year-old adults in its National Immunisation Program from 2016. In November 2023 this was replaced with the recombinant adjuvanted herpes zoster vaccine (RZV, Shingrix) and eligibility expanded to include adults ≥65 years old and immunocompromised adults ≥18 years. We aimed to assess the vaccine program impact and RZV effectiveness in eligible adults.