Pulmonary protein surfactant therapy has been seminal in the improved survival of premature neonates. However, a significant proportion of premature neonates born less than 28 weeks gestation, develop neonatal chronic lung disease. Premature neonatal lungs have not developed the surfactant stores essential for breathing and require surfactant as a replacement therapy. Unfortunately, current commercial surfactant therapies contain only surfactant proteins SP-B and C and lack the essential anti-inflammatory innate immune proteins SP-A and SP-D.
Fifteen million babies are born prematurely every year. Approximately 50% of premature infants born at less than 28 weeks gestation develop chronic lung disease characterized by a dependency on oxygen at 36 weeks gestational age.
These children may develop lung inflammation and require long-term home oxygen therapy for up to 4-5 years, potentially leading to permanent adverse respiratory and neurodevelopmental outcomes. Oxygen therapy may also damage the delicate lung tissue of the premature neonate. Importantly, commercial surfactant formulations which lack the natural anti-inflammatory proteins (SP-A and SP-D) do not protect against this damage. There are currently no effective treatments for neonatal chronic lung disease (nCLD)
SARS-CoV-2 has spread globally and infected millions of people and this number is growing exponentially. However, there are no effective treatments to treat or prevent the disease caused by this virus, do not protect against this damage. Infection with SARS-CoV-2 critically infects alveolar type-II cells, which are the cells that produce the natural lung defence molecule SP-D. SARS-CoV-2 infected individuals develop a cough with fever and in a many of cases subsequently viral pneumonia. Patients with SARS-CoV-2 pneumonia can progress and develop severe acute respiratory distress syndrome (SARS) which require intensive care in ICU. Up to half of those with critical disease currently do not survive.
Recombinant fragment SP-D is well characterised and binds to and neutralises several viruses including Respiratory Syncytial Virus (RSV) and in the same way recognises the coronaviruses which give rise to severe acute respiratory syndrome (SARS). We propose to treat patients with SARS due to coronavirus infection, initially those with SARS-CoV-2 infection, by delivering rfhSP-D directly to their lower respiratory tree.