Infectious Disease Reports 

About: Infectious Disease Reports is an academic journal published by Multidisciplinary Digital Publishing Institute. The journal publishes majorly in the area(s): Medicine & Internal medicine. It has an ISSN identifier of 2036-7430. It is also open access. Over the lifetime, 491 publications have been published receiving 4296 citations.

Tuberculosis 2015: Burden, Challenges and Strategy for Control and Elimination.

Abstract: Tuberculosis (TB) is a leading cause of morbidity and mortality worldwide, accounting for about 9.6 million new cases and 1.5 million deaths annually. The poorest and socially excluded groups carry the largest burden of disease, which makes it essential to properly address the social determinants of health through poverty reduction measures and targeted interventions on high-risk populations. The spread of multidrug-resistance TB requires special attention and highlights the need to foster research on TB diagnostics, new drugs and vaccines. Although many advances have been made in the fight against TB over the last twenty years, a lot is still needed to achieve global elimination. The new end-TB strategy that was first launched in 2014 by the World Health Organization, is fully in line with the seventeen Sustainable Development Goals that came into effect since January 2016 and sets ambitious goals for the post-2015 agenda. A 90% reduction in TB-related mortality and an 80% decline in TB incidence within 2030 as well as the abolition of catastrophic expenditures for TB-affected people are the main targets of this strategy. Strong government commitment and adequate financing from all countries together with community engagement and appropriate investments in research are necessary in order to reach these objectives.

National Institute for the Infectious Diseases "L. Spallanzani", IRCCS. Recommendations for COVID-19 clinical management.

Abstract: On January 9 2020, the World Health Organization (WHO) declared the identification, by Chinese Health authorities, of a novel coronavirus, further classified as SARS-CoV-2 responsible of a disease (COVID-19) ranging from asymptomatic cases to severe respiratory involvement. On March 9 2020, WHO declared COVID-19 a global pandemic. Italy is the second most affected country by COVID-19 infection after China. The "L. Spallanzani" National Institute for the Infectious Diseases, IRCCS, Rome, Italy, has been the first Italian hospital to admit and manage patients affected by COVID-19. Hereby, we show our recommendations for the management of COVID-19 patients, based on very limited clinical evidences; they should be considered as expert opinions, which may be modified according to newly produced literature data.

Tuberculosis Biomarkers: From Diagnosis to Protection

Abstract: New approaches to control tuberculosis (TB) worldwide are needed. In particular, new tools for diagnosis and new biomarkers are required to evaluate both pathogen and host key elements of the response to infection. Non-sputum based diagnostic tests, biomarkers predictive of adequate responsiveness to treatment, and biomarkers of risk of developing active TB disease are major goals. Here, we review the current state of the field. Although reports on new candidate biomarkers are numerous, validation and independent confirmation are rare. Efforts are needed to reduce the gap between the exploratory up-stream identification of candidate biomarkers, and the validation of biomarkers against clear clinical endpoints in different populations. This will need a major commitment from both scientists and funding bodies.

Covid-19 R0: Magic number or conundrum?

Abstract: There is an increasing concern about COVID-19 worldwide. This is a new emerging infectious disease caused by a novel coronavirus (SARS-CoV-2), which recently broke out from the Chinese city of Wuhan and has quickly spread in China, with sporadic cases in each continent.1 At the date of February 20th, 2020, SARS-CoV-2 caused 74 675 infections in China with 2 121 deaths, and 1 073 infections in 26 countries with 8 deaths outside China.1 COVID-19 represents the third coronavirus-associated epidemic to emerge from a species leap from wild animals to humans, after Severe Acute Respiratory Syndrome (SARS) in 2003, and the Middle East Respiratory Syndrome (MERS) in 2012.2,3 SARS-CoV-2 Often causes a respiratory disease, similar to SARS and MERS, ranging from mild upper respiratory illness to a severe interstitial pneumonia, also requiring intensive care.4,5 One of the most discussed issues about COVID-19 is its basic reproduction number (R0). Public opinion and mass media are increasingly focusing on this epidemiological value, often alarming about the spreading potential of this novel infection, defining R0 as a “fatal number”: the more it increases, the greater is the risk for the population, including higher mortality potential. On the other hand, the scientific community has not given a definite and sound response about the real epidemiological potential of COVID-19, to date. Scientists are currently debating about the actual reproductive number of COVID-19 and it is not hard to find sensationalistic statements about the R0 and its impact on the pandemic COVID-19 potential. Indeed, since COVID-19 broke out, several published study aiming to forecast its epidemic trend, have estimated different R0 values, often much higher than that of SARS and MERS. R0 is the average number of secondary infections produced by an infectious case in a population where everyone is susceptible and it is used to measure the transmission potential of a communicable disease.6 When R0 is >1, it means that each individual affected by a transmittable disease is expected to infect a number of subjects that increase exponentially with the increase of the R0 value and the disease is expected to spread through the susceptible population. Conversely, when R0 is <1 each case transmits the disease to one or less than one individual and the disease is expected to die out in the population.6 Although the concept of R0 is very intuitive, its calculation is based on complex models and may lead to misinterpretations, especially for what concerns the real weight that R0 has on the spreading of an infectious disease and on the feasibility of controlling an epidemic.6 The basic reproductive number (R0) of COVID-19 has been initially estimated by the World Health Organization (WHO) to range between 1.4 and 2.5, as declared in the statement regarding the outbreak of SARS-CoV-2, dated 23th January 2020.7 However, several published studies aimed to precisely estimate the COVID-19 R0. A recent review written by Liu et al. compared 12 studies published from the 1st of January to the 7th of February 2020 which have estimated the R0 for COVID19, finding a range of values between 1.5 and 6.68.8 The authors of the review calculated the mean and the median of R0 estimated by the 12 studies and they found a final mean and median value of R0 for COVID-19 of 3.28 and 2.79, respectively, with an interquartile range (IQR) of 1.16.8 According to these findings, the COVID-19 R0 would exceed the reproductive number estimated for SARS.9 The reasons behind a low level of accordance between studies attempting to estimate the R0 are complex and can be attributed to 3 possible reasons: i) different variables considered; ii) different methods for modeling; and iii) different estimation procedures.9 Firstly, R0 is not an intrinsic variable of the infectious agent, but it is calculated through at least three parameters: the duration of contagiousness; the likelihood of infection per contact between; and the contact rate, along with economical, social and environmental factors, that may vary among studies aimed to estimate the R0. More, the use of different models for the estimation of R0 may play a role in the discrepancies observed among the studies on COVID-19. In fact, according to Liu’s findings, the studies using mathematical methods produce estimates that are higher than stochastic and statistic models in determining COVID-19 R0.8 It must be noted that the estimation of R0 assumes that the number of secondary infections produced by a single case has no variations.9 However, super-spreading events, in which a single individual, not necessarily strongly symptomatic, may infect a wide number of subjects, as occurred in the past with SARS and MERS, may occur.10 Recently, a British businessman with COVID-19 has been alleged to transmit the infection to 11 people in a French chalet.11 Therefore, the models used to estimate the R0 cannot fully consider the large heterogeneity in space, transmissibility, and susceptibility of an infection. Additionally, the basic reproductive number is constantly modified during an epidemic by the control measures adopted to reduce the fundamental coefficient of R0, namely: i) the duration of contagiousness; ii) the likelihood of infection per contact; and iii) the contact rate.12 One effective measure is quarantine. During SARS epidemic, several countries introduced the use of mass quarantine for all individuals suspected of having had contact with a confirmed SARS case. These coordinated global efforts were remarkably effective at curtailing the spread of the disease, and this strategy was effective, together with isolation of infected patients and public health measures to contain the epidemic and avoiding SARS reemergence. Another important value that has not received sufficient attention to date is the control reproductive number (Rc) that is the value of R in the presence of control measures. If Rc can be sustained at values below one, then the disease will eventually Infectious Disease Reports 2020; volume 12:8516

Pathogenesis of HIV infection

Abstract: Over the past three decades of intense research on the contribution of viral and host factors determining the variability in HIV-1 infection outcome, HIV pathogenesis is still a fascinating topic that requires further study. An understanding of the exact mechanism of how these factors influencing HIV pathogenesis is critical to the development of effective strate- gies to prevent infection. Significant progress has been made in identifying the role of CCR5 (R5) and CXCR4 (X4) HIV strains in disease progression, particularly with the persistence of R5 HIV-1 strains at the AIDS stage. This indicates that R5 strains are as fit as X4 in causing CD4+ T cell depletion and in contribution to disease outcome, and so questions the prerequisite of the shift from R5 to X4 for disease progression. In contrast, the ability of certain HIV strains to readily use CXCR4 for infection or entry into macrophages, as the case with viruses are homozygous for tropism by CCR5delta32. This raises another major paradox in HIV pathogenesis about the source of X4 variants and how do they emerge from a relatively homogeneous R5 viral population after transmission. The interactions between viral phenotypes, tropism and co-receptor usage and how they influence HIV pathogenesis are the main themes addressed in this review. A better understanding of the viral and host genetic factors involved in the fitness of X4 and R5 strains of HIV-1 may facilitate development of specific inhibitors against these viral populations to at least reduce the risk of disease progression.