On Thursday, Uganda confirmed an outbreak of the Ebola virus in its capital city Kampala, with the first confirmed patient dying from it a day before. As per the new developments, the officials are now preparing to deploy a trial vaccine to put an end to this outbreak.
Groups of scientists are working on the vaccine and deployment of more than 2,000 doses of a candidate vaccine against the Sudan strain of Ebola has been planned and confirmed by the Uganda Virus Research Institute. As per the World Health Organization (WHO), Uganda has access to 2,169 doses of trial vaccine. For now, however, there are no approved vaccines for the strain and officials are still investigating the source of the outbreak.
The WHO had also allocated $1 million from its contingency fund for emergencies to support quick action and contain the outbreak in the country.
On Wednesday, the Sudan strain of Ebola killed a nurse employed at Kampala's main referral hospital. It is after his death that Ebola was declared an outbreak in the country. Post-mortem samples too have confirmed the Sudan Ebola Virus Disease and at least 44 contacts of the deceased man have been listed for tracing. 30 of these are health workers.
Ebola is a highly infectious hemorrhagic fever, which is transmitted through contact with bodily fluids and tissue. Symptoms include headache, vomiting of blood, muscle pains and bleeding.
it was in the late 2022, when Uganda had last suffered an Ebola outbreak. It killed 55 of the 143 people who were infected and was declared over on January 11, 2023.
As per the WHO, Ebola virus disease (EVD) is a rare but severe illness in humans and is often fatal. People can get infected with the virus if they touch an infected animal when preparing food, or touch body fluids of an infected person such as saliva, urine, faeces or semen, or things that have body fluids of an infected person like clothes or sheets.
Ebola enters the body through cuts in the skin or when one is touching their eyes, nose or mouth. Early symptoms include fever, fatigue and headache.
It was first discovered in 1976 in two simultaneous outbreak, when in Nzara, South Sudan and other in Yambuku, Democratic Republic of Congo. The latter occurred near a village near the Ebola River, which is where it gets its name from.
It is highly infectious and transmissible disease, in fact, there have been cases of health-care workers who have frequently been infected while treating patients with suspected or confirmed Ebola. This occurs through close contact with patients when infection control precautions are not practiced strictly.
Cases of people conducted burial ceremonies, involving direct contact with the body of the deceased too can lead to the transmission of Ebola. Even after the long suffering and recovery, there is a possibility of sexual transmission. Pregnant women who get acute Ebola and recover may still carry the virus in their breastmilk, or in pregnancy related fluids and tissues.
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Quitting smoking remains one of the best decisions for your health. But new research suggests that even years after your last cigarette, your lungs may continue to carry the harmful effects that increase the risk of chronic lung disease.
A new study by McGill University, published in the journal Translational Research, finds why former smokers remain at high risk to lung diseases even after quitting.
By analysing lung cells closely, scientists found that even though some damage due to smoking heals over time, other damages persist, leaving ex-smokers at a higher risk of conditions like chronic obstructive pulmonary disease (COPD) and lung cancer.
The study was conducted on more than 100,000 individual lung cells collected from 21 people, including nine people who had never smoked, five active smokers, and seven former smokers.
Using single-cell RNA sequencing, researchers examined molecular activity across more than 40 different lung cell types, creating one of the most comprehensive maps of how smoking and smoking cessation affect the lungs at the cellular level.
Their findings revealed that long-term lung recovery is not uniform. While some lung cells gradually regained healthier patterns after smoking cessation, others continued to show long-term molecular changes affecting tissues, immune responses, blood vessel function, and the overall lung health.
Perhaps the most surprising finding was that some cells in ex-smokers showed unique molecular markers that were not seen in active smoker and participants who never smoked, suggesting quitting smoking creates its own biological impact.
Also read: Even Light Exercise Could Help People With COPD Live Longer, Study Finds
Scientists have long known that the risk of lung cancer and COPD declines after quitting smoking, but it never completely returns to the same level as seen in people who have never touched a cigarette.
Smoking damages DNA, alters gene activity, triggers chronic inflammation and injures delicate lung tissues. While the body repairs some of this damage after the smoker quits, certain cellular changes become persistent.
These lingering molecular alterations could continue influencing how lung tissue responds to injury, infections and aging.
Senior author Professor Carolyn Baglole, from McGill University's Department of Pharmacology and Therapeutics, said, "Current smokers have the highest risk of deadly diseases like lung cancer, but former smokers still face a higher risk than people who never smoked. Despite more than a century of research on smoking, we don't fully understand why."
She added, "Our findings show that while some damage appears reversible, other changes persist long after people stop smoking."
First author Nicole Heimbach, a doctoral student at McGill University, said, "These findings are an important step toward understanding what damage caused by smoking can heal and what may be permanent. By knowing what damage remains after quitting, we can better understand how smoking-related diseases develop and how to treat them."
Also read: Could Wildfire Smoke Trigger Your Migraine? Latest Study Finds A Strong Link
Instead of quitting smoking, if you are thinking of switching to vaping, think again. According to a new study, vape users presented reduced fitness and impaired blood vessel function similar to traditional cigarette smokers.
The research, published in the peer-reviewed journal ERJ Open Research, compared healthy adults aged 18 to 30 and found that both regular vapers and smokers had around 15% lower exercise capacity than people who had never smoked or vaped.
This suggests that electronic cigarettes like vapes are not lesser of two evils.
The researchers, however, caution that the study does not suggest that vaping is equally harmful as smoking in every respect.
Traditional cigarettes still strongly remain linked to major disorders like cancer, chronic obstructive pulmonary disease (COPD), and many other life-threatening illnesses.
But the new study indicates that when it comes to cardiovascular fitness, breathing efficiency, lung function and blood vessel health in young adults, vaping may offer far less protection.
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People who use cannabis frequently believing it relieves stress are about to be proven wrong. A new study debunked the myth that marijuana helps alleviate stress levels.
In fact, researchers recently found that frequent cannabis users may face the risk of higher levels of cortisol, body's stress hormone.
While the study does not prove that marijuana causes chronic stress, they raise important questions about how regular cannabis use affects long-term mental and physical health.
The study, conducted by researchers at Oregon State University and published in the journal Cannabis, examined 82 young adults, including 39 frequent cannabis users and 43 non-users.
Participants provided saliva samples immediately after waking and again 30 minutes later, allowing researchers to measure the cortisol awakening response (CAR), a natural surge in cortisol that prepares the body for the day.
The researchers found that frequent cannabis users had higher cortisol levels immediately upon waking compared to non-users. However, both groups showed a similar cortisol increase during the first 30 minutes after waking.
This suggests that cannabis users started the day with an already elevated stress hormone level rather than having an exaggerated morning cortisol surge.
Also read: 10 Odd Signs Of Stress That You Thought You Knew But Don't
Cortisol, often called the stress hormone, plays several essential roles in the body. It helps regulate:
A temporary rise in cortisol is normal and even beneficial. But, chronically elevated cortisol has been linked to anxiety, depression, cardiovascular disease, metabolic disorders, and impaired immune function.
Many users experience short-term relaxation after consuming marijuana, particularly due to THC's effects on the brain's cannabinoid receptors.
However, researchers say repeated exposure may gradually alter the hypothalamic-pituitary-adrenal (HPA) axis, the body's central stress-response network.
Over time, this could interfere with normal stress regulation, potentially creating a cycle where people increasingly rely on cannabis to cope with stress while their biological stress system becomes dysregulated.
However, researchers clarify that the study does not establish that frequent marijuana use directly causes increase in cortisol.
Also read: Could Wildfire Smoke Trigger Your Migraine? Latest Study Finds A Strong Link
The findings add to a growing body of evidence suggesting that heavy cannabis consumption may have complex effects on mental health. Recent research has linked it with:
Many people use marijuana to unwind after a stressful day, but this study suggests that frequent cannabis use may be associated with higher baseline stress hormone levels upon waking. This could affect one's day-to-day quality of life.
As cannabis use continues to rise worldwide, researchers say understanding its long-term effects on mental health and the body's stress response will be increasingly important, especially to bust common myths associated to its use.
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Long COVID—a debilitating condition that can persist for months or even years after a SARS-CoV-2 infection—may be preventable if treatment begins early, according to a new study.
Long COVID is an infection-associated chronic condition marked by fatigue, cognitive impairment, exercise intolerance, and multisystem dysfunction. It has affected an estimated 400 million people worldwide and continues to have significant health, social, and economic consequences. Despite the ongoing risk, prevention strategies have received relatively little attention.
Now, a landmark randomized trial, published in The Lancet, provides some of the strongest evidence to date that early treatment with the antiviral drug Paxlovid (nirmatrelvir–ritonavir) can reduce the risk of developing Long COVID by 40%. The treatment was effective when started during the acute phase of COVID-19.
“The message is profound: what happens in the first few days of COVID-19 may determine health for months—or even years,” said researchers from the University of California, San Francisco.
The researchers added that preventing Long COVID "may become the next frontier in COVID care."
Paxlovid combines two antiviral medicines—nirmatrelvir and ritonavir—and remains one of the most effective outpatient treatments for people at high risk of severe COVID-19.
Researchers conducted a randomized controlled trial in Norway involving patients with acute COVID-19. They found that a five-day course of nirmatrelvir–ritonavir significantly reduced the risk of Long COVID three months after infection.
For the study, Long COVID was defined as patient-reported fatigue, shortness of breath (dyspnea), or cognitive symptoms during the post-acute phase.
The findings provide some of the first randomized trial evidence that antiviral treatment during acute infection can lower the risk of Long COVID, supporting earlier observational studies.
Importantly, the trial was conducted during the circulation of successive Omicron subvariants, from XBB to LP.8.1, making the findings relevant to the current phase of the pandemic.
A notable finding was the high rate of Long COVID among participants. In the placebo group, 33 of 77 participants (43%) met the criteria for Long COVID despite widespread vaccine-derived immunity. While vaccination offers partial protection, the study suggests a substantial risk still remains.
The researchers suggest several biological mechanisms that may explain the protective effect of early antiviral treatment:
Reducing viral replication early may lower peak viral load and shorten viral shedding, both of which have been linked to Long COVID.
Early treatment may limit immune dysregulation, allowing the body's antiviral immune response to control the virus more effectively.
Treating the infection during its acute phase may prevent or reduce processes associated with Long COVID, including persistent SARS-CoV-2 infection, herpesvirus reactivation, and immune dysfunction.
The trial suggests that early viral replication may trigger "self-sustaining or persistent harmful biological processes" that contribute to Long COVID.
"Defining these relationships could yield predictive biomarkers and more targeted prevention strategies," the researchers noted.
The researchers noted that nirmatrelvir–ritonavir commonly causes dysgeusia (altered taste), which may have influenced how some participants perceived their treatment and reported symptoms. They said future studies should evaluate this possibility and investigate antivirals with less distinctive side-effect profiles.
Other common side effects include diarrhea and high blood pressure (hypertension).
According to the US Food and Drug Administration (FDA), Paxlovid can also interact with several commonly used medications, including statins. Patients should discuss all prescription drugs, over-the-counter medicines, and supplements they are taking with their healthcare provider before starting treatment.
While the current study assessed participants three months after infection, the researchers said longer follow-up is needed to determine whether early antiviral treatment provides durable protection against Long COVID or simply accelerates recovery from acute illness. They also emphasized the need for larger studies to evaluate its impact on severe, disabling forms of Long COVID.
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