Virus World

After months of data collection, scientists agree: The delta variant is the most contagious version of the coronavirus worldwide. It spreads about 225% faster than the original version of the virus, and it's currently dominating the outbreak in the United States. A new study, published online Wednesday, sheds light on why. It finds that the variant grows more rapidly inside people's respiratory tracts and to much higher levels, researchers at the Guangdong Provincial Center for Disease Control and Prevention reported. On average, people infected with the delta variant had about 1,000 times more copies of the virus in their respiratory tracts than those infected with the original strain of the coronavirus, the study reported. In addition, after someone catches the delta variant, the person likely becomes infectious sooner. On average, it took about four days for the delta variant to reach detectable levels inside a person, compared with six days for the original coronavirus variant. 

In the study, scientists analyzed COVID-19 patients involved in the first outbreak of the delta variant in mainland China, which occurred between May 21 and June 18 in Guangzhou, the capital of Guangdong province. The researchers measured the levels of virus in 62 people involved in that outbreak and compared them with the levels in 63 patients infected in 2020 with an early version of the virus. Their findings suggest that people who have contracted the delta variant are likely spreading the virus earlier in the course of their infection. And the scientists underscore the importance of quarantining immediately for 14 days after coming into contact with someone diagnosed with COVID-19, as the U.S. Centers for Disease Control and Prevention recommends.  Or even better, getting fully vaccinated. Preliminary data shows that in some U.S. states, 99.5% of COVID-19 deaths in the past few months were among people who weren't vaccinated, the CDC's director, Dr. Rochelle Walensky, said Thursday at the White House.  "We know that the delta variant ... is currently surging in pockets of the country with low vaccination rates," Walensky said. "We also know that our authorized vaccines prevent severe disease, hospitalization and death from the delta variant."

Study cited available in Virological (July 7, 2021):

https://virological.org/t/viral-infection-and-transmission-in-a-large-well-traced-outbreak-caused-by-the-delta-sars-cov-2-variant/724 

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) detection platforms currently report qualitative results. However, technology based on RT-PCR allows for calculation of viral load, which is associated with transmission risk and disease severity in other viral illnesses. Viral load in COVID-19 might correlate with infectivity, disease phenotype, morbidity, and mortality. To date, no studies have assessed the association between viral load and mortality in a large patient cohort. To our knowledge, we are the first to report on SARS-CoV-2 viral load at diagnosis as an independent predictor of mortality in a large hospitalised cohort (n=1145).

We prospectively evaluated nasopharyngeal swab samples for SARS-CoV-2 by real-time RT-PCR (Roche cobas 6800; Roche, Basel, Switzerland). Positive samples were assessed by a laboratory-developed quantitative RT-PCR test approved for clinical use  and viral loads were calculated with standard curves. Viral loads for symptomatic, hospitalised patients who tested positive for SARS-CoV-2 were measured on samples collected between March 13 and May 4, 2020, that tested positive on both platforms at diagnosis. Only patients with complete survival data (discharged from or died in hospital) were included in our analysis (n=1145). Mean age was 64·6 years (SD 17·5), with 651 (56·9%) male patients, and a self-reported racial distribution of 357 (31·2%) African American patients, 335 (29·3%) white patients, 42 (3·7%) Asian patients, 375 (32·8%) patients of other race, and 36 (3·1%) patients of unknown race. The overall mean log10 viral load was 5·6 copies per mL (SD 3·0), and median log10 viral load was 6·2 copies per mL (IQR 3·0–8·0). Mean log10 viral load significantly differed between patients who were alive (n=807; mean log10 viral load 5·2 copies per mL [SD 3]) versus those who had died (n=338; 6·4 copies per mL [2·7]) by the end of the study period.

A Cox proportional hazards model adjusting for age, sex, asthma, atrial fibrillation, coronary artery disease, chronic kidney disease, chronic obstructive pulmonary disease, diabetes, heart failure, hypertension, stroke, and race yielded a significant independent association between viral load and mortality (hazard ratio 1·07 [95% CI 1·03–1·11], p=0·0014; appendix p 3), with a 7% increase in hazard for each log transformed copy per mL. A univariate survival analysis revealed a significant difference in survival probability between those with high viral load (defined as being greater than the overall mean log10 viral load of 5·6 copies per mL) and those with low viral load (p=0·0003; appendix p 4), with a mean follow-up of 13 days (SD 11) and a maximum follow-up of 67 days.

Published at the Lancet (August 6, 2020):

https://doi.org/10.1016/S2213-2600(20)30354-4

Coronavirus disease 2019 (COVID-19) is a new pandemic disease. We previously reported that the viral load of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) peaks within the first week of disease onset.1,2 Findings from Feb, 2020, indicated that the clinical spectrum of this disease can be very heterogeneous.3 Here, we report the viral RNA shedding patterns observed in patients with mild and severe COVID-19...

HIV BREAKTHROUGH - Genetic study identifies Africa-specific variant near CHD1L gene associated with lower HIV-1 viral load in populations of African descent. New research has found a genetic variant that may explain why some people of African ancestry have naturally lower viral loads of HIV, reducing their risk of transmitting the virus and slowing progress of their own illness. The paper, published today in Nature, demonstrates the first new genetic variant related to HIV infection discovered in nearly 30 years of research. It could, in the future, help direct the development of new treatments and approaches for those living with HIV. HIV-1 remains a significant global health crisis, and identifying new targets for therapies is crucial. The study focuses on individuals of African descent due to the disproportionate burden of HIV-1 in Africa and the high genetic diversity in the region. An international team of researchers analysed the DNA of almost 4,000 people of African ancestry living with HIV-1, the most common type of the virus. They identified a variant within a region on chromosome 1 containing the gene CHD1L which is associated with reduced viral load in carriers of the variant. Between 4% and 13 % of people of African origin are thought to carry this particular variant.  Viral load is the amount of a virus in a patient’s system. Higher levels are known to correlate with faster disease progression and increased risk of transmission. But viral load varies widely among infected individuals, influenced by a number of factors including an individual’s genetic makeup. Co-Senior author Professor Manjinder Sandhu, Chair in Population Health and Data Science in the School of Public Health, said: “With more than a million new HIV infections a year, it’s clear that we still have a long way to go in the fight against HIV – we are yet to have a vaccine to prevent infection, have yet to find a cure and still see drug resistance emerging in some individuals. The next step is to fully understand exactly how this genetic variant controls HIV replication.”

Understanding African populations

Most of what we know about the relationship between our DNA and HIV comes from studies among European populations. But given that HIV disproportionately affects people on the African continent – more than 25 million people who are HIV-positive live on the continent – it’s important to better understand the role of genetics in HIV infection in African populations.  Paul McLaren from the Public Health Agency of Canada’s National Microbiology Laboratory and joint first author on the paper, said: “African populations are still drastically underrepresented in human DNA studies, despite experiencing the highest burden of HIV infection. By studying a large sample of people of African ancestry, we’ve been able to identify a new genetic variant that only exists in this population and which is linked to lower HIV viral loads.”

Reducing viral load

CHD1L is known to play a role in repairing damaged DNA, though it is not clear why the variant should be important in reducing viral load. However, as HIV attacks immune cells, researchers at the University of Cambridge’s Department of Medicine, led by Dr Harriet Groom and Professor Andrew Lever, used stem cells to generate variants of cells that HIV can infect in which CHD1L had either been switched off or its activity turned down. HIV turned out to replicate better in a type of immune cell known as a macrophage when CHD1L was switched off. In another cell type, the T cell, there was no effect – perhaps surprising since most HIV replication occurs in the latter cell type.  Dr Harriet Groom said: “This gene seems to be important to controlling viral load in people of African ancestry. Although we don’t yet know how it’s doing this, every time we discover something new about HIV control, we learn something new about the virus and something new about the cell. The link between HIV replication in macrophages and viral load is particularly interesting and unexpected.

Original study published (August 2, 2023) in Nature:

https://doi.org/10.1038/s41586-023-06370-4 

Preliminary results from an Israel-based study suggest that one dose of the vaccine reduces infectiousness—a key factor in slowing virus spread. People who became infected with SARS-CoV-2 after receiving one dose of Pfizer’s COVID-19 vaccine harbored about four times less virus than did unvaccinated people who caught the virus, according to preliminary results posted to the preprint server medRxiv on February 8. Several COVID-19 vaccines, including Pfizer’s version, are about 95 percent effective in preventing disease. But there’s less known about whether vaccinated individuals can still transmit the SARS-CoV-2 virus to others.  In the study, which has not yet undergone peer review, researchers in Israel measured the viral loads in 2,897 unvaccinated people and in 2,897 age- and sex-matched people who had received their first of two doses of the Pfizer vaccine. The authors conclude in their report that “viral load is reduced 4-fold for infections occurring 12–28 days after the first dose of vaccine. These reduced viral loads hint to lower infectiousness, further contributing to vaccine impact on virus spread.”  Viral abundance could drop further after the vaccine’s second dose, Cyrille Cohen, a vaccine expert at Bar-Ilan University who advises Israel’s health ministry on COVID-19 vaccines and wasn’t involved with the study, tells The Times of Israel. “This is a game-changer to some extent,” he says. “After all, transmissibility after the vaccine has been one of the most important questions we are asking ourselves.”

Israel’s rollout of the Pfizer vaccine is among the most effective COVID-19 vaccination programs in the world, according to Reuters. The country started its vaccine drive, which initially targeted older and at-risk groups, on December 19. Since then, more than half of its eligible population—about 3.5 million people—have received one or both doses.  Already, some results from Israel’s vaccination efforts have emerged, Reuters reports. In people aged over 60—the group prioritized for vaccinations—there was a 53 percent drop in new cases between January 16 and February 6. Hospitalization and severe cases have also declined by more than 30 percent in this age group. In those aged younger than 60—who became eligible for the vaccine later—there was a 20 percent reduction in new cases during the same period, but hospitalizations and severe cases rose by 15 and 29 percent, respectively. Reuters did not provide an explanation for opposing trends in the younger group. Pfizer’s vaccine appears to retain its 90–95 percent effectiveness against the highly transmissible B.1.1.7 variant, which was first detected in the UK and is rapidly spreading around the world, Hezi Levi, the director-general of the Israeli Health Ministry, tells Reuters. “It’s too early to say anything about the South African variant.”

See preprint available in medRxiv (Feb. 8, 2020):

https://doi.org/10.1101/2021.02.06.21251283

Researchers in South Korea found that roughly 30 percent of those infected never develop symptoms yet probably spread the virus. Of all the coronavirus’s qualities, perhaps the most surprising has been that seemingly healthy people can spread it to others. This trait has made the virus difficult to contain, and continues to challenge efforts to identify and isolate infected people. Most of the evidence for asymptomatic spread has been based on observation (a person without symptoms nevertheless sickened others) or elimination (people became ill but could not be connected to anyone with symptoms). A new study in South Korea, published Thursday in JAMA Internal Medicine, offers more definitive proof that people without symptoms carry just as much virus in their nose, throat and lungs as those with symptoms, and for almost as long.  “It’s important data, that’s for sure,” said Benjamin Cowling, an epidemiologist at the University of Hong Kong who was not involved in the work. “And it does confirm what we’ve suspected for a long time — that asymptomatic cases can transmit infection.”