Oral Cavity Serves as Long-Term COVID-19 Reservoir with Increased Periodontal and Viral Disease Risk:
-COVID-19 history significantly correlates with severe oral health complications while vaccination reduced but did not eliminate these issues. 1/
A NEW study identified oral associated #LonhCovid primarily manifested as periodontal (gum) disease (COVID +ve: 73.1±18.9% vs COVID -ve: 33.1±14.3%)
Covid19 positive cases correlated w/ higher rates of dry mouth (57.5%), taste disturbance (47%) & smell loss (20%). 2/
Vaccination reduced oral LongCovid (PASC) in COVID-19 positive subjects; however, periodontal disease indicators persisted compared to the COVID-19 negative group. 3/
Notably, 3-6 months post-infection, while SARS-CoV-2 Spike (S) transcript was rarely detected in saliva (∼6%), its protein was commonly detected (∼70%) in the COVID-19 positive subjects indicating incomplete viral clearance. 4/
This correlates with significantly higher salivary expression of viral entry receptors (ACE2, and TRMPSS2), and inflammatory mediators (IL-6, IL-8 and MMP-8), in COVID-19 positive subjects. 5/
This finding was further supported by higher prevalence of other oral viruses including Epstein-Barr Virus (70.5%), Herpes Simplex Virus (8.1%), and Human Papillomavirus (17.5%) in COVID-19 positive subjects. 6/6
New study in International Journal of Infectious Diseases highlights persistent immune alterations after SARS-CoV-2 infection—providing further biological evidence for #LongCOVID as a genuine post-infectious condition.
➡️ Researchers found lasting changes in immune activation and regulation, even months after recovery from acute COVID-19—suggesting the immune system does not fully reset after infection. 1/
Key findings point to chronic inflammation, altered cytokine responses, and immune imbalance, which may explain prolonged symptoms such as fatigue, pain, and neurocognitive complaints.
➡️ Importantly, these immune changes were seen independent of initial disease severity, reinforcing that even mild COVID-19 can have long-term immunological consequences. 2/
The study of >40,000 people shows that key immune cells (T cells, B cells, NK cells) dropped during widespread COVID infection and stayed below pre-pandemic levels for nearly 2 years. 3/
A new Israeli study demonstrates why some people develop #LongCOVID.
➡️ By analysing immune responses, gene expression and plasma proteins in blood samples, scientists found that people with longCOVID show persistent chronic inflammation and disrupted immune signalling months after infection — patterns not seen in those who fully recovered. 1/
These immune differences help explain lingering symptoms — such as fatigue, brain fog and breathlessness — and point to specific inflammatory pathways that could be targeted for treatment. This work opens new avenues for better therapies for millions living with longCOVID. 2/
Researchers performed immunological, virological, transcriptomic and proteomic analyses from a cohort of 142 individuals between 2020 and 2021, including uninfected controls (n = 35), acutely infected individuals (n = 54), convalescent controls (n = 24) and patients with LC (n = 28).
➡️ The LC group was characterized by persistent immune activation and proinflammatory responses for more than 180 days after initial infection compared with convalescent controls, including upregulation of JAK-STAT, interleukin-6, complement, metabolism and T cell exhaustion pathways.
➡️ Similar findings were observed in a second cohort enrolled between 2023 and 2024, including convalescent controls (n = 20) and patients with LC (n = 18). 3/
Can past COVID-19 weaken the body’s ability to fight tuberculosis?
➡️ A new study comparing immune responses to SARS-CoV-2 and Mycobacterium tuberculosis (MTB) suggests COVID-19 may dampen both antiviral and anti-TB immunity — even months later. 1/
Researchers tested immune cells from healthy individuals and COVID-19 survivors, both with and without latent TB infection (LTBI).
➡️ They stimulated the cells with SARS-CoV-2 Spike and MTB antigens and measured cytokine responses. 2/
Key finding:
➡️ People who recovered from COVID-19 showed significantly reduced inflammatory cytokines — IFN-γ, IL-2, IL-6, TNF-α — in response to both SARS-CoV-2 and MTB antigens.
➡️ Suggests prolonged immune downregulation after COVID-19. 3/
A new study comparing immune profiles months after COVID-19 vs influenza shows that SARS-CoV-2 leaves behind distinct and longer-lasting immune abnormalities — very different from what is seen after flu. 1/
Post-COVID patients showed increased CXCR3 and CCR6 expression across multiple lymphocyte populations.
➡️ Punjabi This means their immune system is still sending signals for cells to migrate into tissues (especially the lungs) months after infection.
In contrast, post-flu patients mainly showed a decrease in CCR4 on naïve T cells, monocytes, and dendritic cells — a very different and less persistent pattern.
➡️ Flu does not drive the same long-term immune activation. 3/
A new study provides some of the strongest evidence yet that mitochondrial dysfunction can directly cause #Parkinson’s disease, rather than being a consequence of neuron loss.
➡️ Researchers used a unique mouse model carrying a mutation in CHCHD2, a mitochondrial protein linked to a rare inherited form of Parkinson’s that closely mimics the common, late-onset form. 1/
Key Findings
➡️ Mutant CHCHD2 accumulates in mitochondria, making them swollen and structurally abnormal.
➡️ Cells shift away from normal energy production and develop oxidative stress due to buildup of reactive oxygen species (ROS).
➡️ Alpha-synuclein aggregation occurs after ROS rises, suggesting oxidative stress triggers Lewy body formation.
➡️ Human brain tissue from people with sporadic Parkinson’s showed CHCHD2 accumulation inside early alpha-synuclein aggregates, confirming relevance beyond the rare genetic form. 2/
Implications
➡️ This work maps a step-by-step causal chain:
CHCHD2 mutation → mitochondrial failure → metabolic shift → ROS buildup → alpha-synuclein aggregation → Parkinson’s pathology
➡️ It supports the idea that mitochondrial defects may underlie many forms of Parkinson’s, not just the inherited type.
➡️ Targeting oxidative stress, mitochondrial health, and energy pathways could offer new therapeutic strategies. 3/
New research in Cell Reports Medicine helps explain why women are more likely to develop #LongCOVID — and often experience more severe, persistent symptoms like fatigue, brain fog, and pain.
The key? Differences in the immune system, gut, and hormones. 1/
Researchers studied 78 people with LongCOVID (mostly mild initial cases) and compared them to 62 who recovered fully.
➡️ One year later, women with Long COVID showed clear biological differences — especially signs of gut inflammation and “leakiness.” 2/
The study also found anemia and hormone imbalances.
Women with LongCOVID had lower testosterone — a hormone that normally helps control inflammation.
➡️ Lower testosterone was linked to more fatigue, pain, brain fog, and depression. 3/